5.1 Overall goals

5.1.1 Background

Population nutrient intake goals represent the population
average intake that is judged to be consistent with the maintenance of health in
a population. Health, in this context, is marked by a low prevalence of
diet-related diseases in the population.

Seldom is there a single best value for such a
goal. Instead, consistent with the concept of a safe range of nutrient intakes
for individuals, there is often a range of population averages that would be
consistent with the maintenance of health. If existing population averages fall
outside this range, or trends in intake suggest that the population average will
move outside the range, health concerns are likely to arise. Sometimes there is
no lower limit; this implies that there is no evidence that the nutrient is
required in the diet and hence low intakes should not give rise to concern. It
would be of concern if a large proportion of values were outside the defined
goals.

5.1.2 Strength of
evidence

Ideally the definition of an increased or a decreased risk
should be based on a relationship that has been established by multiple
randomized controlled trials of interventions on populations that are
representative of the target of a recommendation, but this type of evidence is
often not available. The recommended dietary/nutrition practice should modify
the attributable risk of the undesirable exposure in that population.

The following criteria are used to describe the strength of
evidence in this report. They are based on the criteria used by the World Cancer
Research Fund (1), but have been modified by the Expert Consultation to
include the results of controlled trials where relevant and available. In
addition, consistent evidence on community and environmental factors which lead
to behaviour changes and thereby modify risks has been taken into account in
categorizing risks. This applies particularly to the complex interaction between
environmental factors that affect excess weight gain, a risk factor which the
Consultation recognized as contributing to many of the problems being
considered.

Convincing
evidence. Evidence based on epidemiological studies showing consistent
associations between exposure and disease, with little or no evidence to the
contrary. The available evidence is based on a substantial number of studies
including prospective observational studies and where relevant, randomized
controlled trials of sufficient size, duration and quality showing consistent
effects. The association should be biologically plausible.

Probable evidence.
Evidence based on epidemiological studies showing fairly consistent
associations between exposure and disease, but where there are perceived
shortcomings in the available evidence or some evidence to the contrary, which
precludes a more definite judgement. Shortcomings in the evidence may be any of
the following: insufficient duration of trials (or studies); insufficient trials
(or studies) available; inadequate sample sizes; incomplete follow-up.
Laboratory evidence is usually supportive. Again, the association should be
biologically plausible.

Possible evidence.
Evidence based mainly on findings from case-control and cross-sectional
studies. Insufficient randomized controlled trials, observational studies or
non-randomized controlled trials are available. Evidence based on
non-epidemiological studies, such as clinical and laboratory investigations, is
supportive. More trials are required to support the tentative associations,
which should also be biologically plausible.

Insufficient evidence.
Evidence based on findings of a few studies which are suggestive, but are
insufficient to establish an association between exposure and disease. Limited
or no evidence is available from randomized controlled trials. More well
designed research is required to support the tentative associations.

The strength of evidence linking dietary and lifestyle factors
to the risk of developing obesity, type 2 diabetes, CVD, cancer, dental
diseases, osteoporosis, graded according to the above categories, is summarized
in tabular form, and attached to this report as an Annex.

5.1.3 A summary of population nutrient
intake goals

The population nutrient intake goals for consideration by
national and regional bodies establishing dietary recommendations for the
prevention of diet-related chronic diseases are presented in Table 6. These
recommendations are expressed in numerical terms, rather than as increases or
decreases in intakes of specific nutrients, because the desirable change will
depend upon existing intakes in the particular population, and could be in
either direction.

In Table 6, attention is directed towards the energy-supplying
macronutrients. This must not be taken to imply a lack of concern for the other
nutrients. Rather, it is a recognition of the fact that previous reports issued
by FAO and WHO have provided limited guidance on the meaning of a balanced
diet described in terms of the proportions of the various energy sources,
and that there is an apparent consensus on this aspect of diet in relation to
effects on the chronic non-deficiency diseases.

This report therefore complements these existing reports on
energy and nutrient requirements issued by FAO and WHO (2-4). In
translating these goals into dietary guidelines, due consideration should be
given to the process for setting up national dietary guidelines
(5).

b The percentage of total energy available after
taking into account that consumed as protein and fat, hence the wide
range.

c The term free sugars refers to all
monosaccharides and disaccharides added to foods by the manufacturer, cook or
consumer, plus sugars naturally present in honey, syrups and fruit
juices.

d The suggested range should be seen in the light
of the Joint WHO/FAO/UNU Expert Consultation on Protein and Amino Acid
Requirements in Human Nutrition, held in Geneva from 9 to 16 April 2002
(2).

e Salt should be iodized appropriately (6).
The need to adjust salt iodization, depending on observed sodium intake and
surveillance of iodine status of the population, should be recognized.

f See page 58, under Non-starch
polysaccharides.

Total fat

The recommendations for total fat are formulated to include
countries where the usual fat intake is typically above 30% as well as those
where the usual intake may be very low, for example less than 15%. Total fat
energy of at least 20% is consistent with good health. Highly active groups with
diets rich in vegetables, legumes, fruits and wholegrain cereals may, however,
sustain a total fat intake of up to 35% without the risk of unhealthy weight
gain.

For countries where the usual fat intake is between 15% and
20% of energy, there is no direct evidence for men that raising fat intake to
20% will be beneficial (7, 8). For women of reproductive age at least 20%
has been recommended by the Joint FAO/WHO Expert Consultation on Fats and Oils
in Human Nutrition that met in 1993 (3).

Free sugars

It is recognized that higher intakes of free sugars threaten
the nutrient quality of diets by providing significant energy without specific
nutrients. The Consultation considered that restriction of free sugars was also
likely to contribute to reducing the risk of unhealthy weight gain, noting
that:

Free sugars
contribute to the overall energy density of diets.

Free sugars promote a positive
energy balance. Acute and short-term studies in human volunteers have
demonstrated increased total energy intake when the energy density of the diet
is increased, whether by free sugars or fat (9-11). Diets that are
limited in free sugars have been shown to reduce total energy intake and induce
weight loss (12, 13).

Drinks that are rich in free
sugars increase overall energy intake by reducing appetite control. There is
thus less of a compensatory reduction of food intake after the consumption of
high-sugars drinks than when additional foods of equivalent energy content are
provided (11, 14-16). A recent randomized trial showed that when soft
drinks rich in free sugars are consumed there is a higher energy intake and a
progressive increase in body weight when compared with energy-free drinks that
are artificially sweetened (17). Children with a high consumption of soft
drinks rich in free sugars are more likely to be overweight and to gain excess
weight (16).

The Consultation recognized that a population goal for free
sugars of less than 10% of total energy is controversial. However, the
Consultation considered that the studies showing no effect of free sugars on
excess weight have limitations. The CARMEN study (Carbohydrate Ratio Management
in European National diets) was a multicentre, randomized trial that tested the
effects on body weight and blood lipids in overweight individuals of altering
the ratio of fat to carbohydrate, as well as the ratio of simple to complex
carbohydrate per se. A greater weight reduction was observed with the high
complex carbohydrate diet relative to the simple carbohydrate one; the
difference, however was not statistically significant (18). Nevertheless,
an analysis of weight change and metabolic indices for those with metabolic
syndrome revealed a clear benefit of replacing simple by complex carbohydrates
(19). The Consultation also examined the results of studies that found an
inverse relationship between free sugars intakes and total fat intake. Many of
these studies are methodologically inappropriate for determining the causes of
excess weight gain, since the percentage of calories from fat will decrease as
the percentage of calories from carbohydrates increases and vice versa.
Furthermore, these analyses do not usually distinguish between free sugars in
foods and free sugars in drinks. Thus, these analyses are not good predictors of
the responses in energy intake to a selective reduction in free sugars
intake.

Non-starch polysaccharides (NSP)

Wholegrain cereals, fruits and vegetables are the preferred
sources of non-starch polysaccharides (NSP). The best definition of dietary
fibre remains to be established, given the potential health benefits of
resistant starch. The recommended intake of fruits and vegetables (see below)
and consumption of wholegrain foods is likely to provide >20 g per day of NSP
(>25 g per day of total dietary fibre).

Fruits and vegetables

The benefit of fruits and vegetables cannot be ascribed to a
single or mix of nutrients and bioactive substances. Therefore, this food
category was included rather than the nutrients themselves. The category of
tubers (i.e. potatoes, cassava) should not be included in fruits and
vegetables.

Body mass index (BMI)

The goal for body mass index (BMI) included in this report
follows the recommendations made by the WHO Expert Consultation on Obesity that
met in 1997 (20). At the population level, the goal is for an adult
median BMI of 21-23 kg/m2. For individuals, the recommendation is to maintain a
BMI in the range 18.5-24.9 kg/m2 and to avoid a weight gain greater than 5 kg
during adult life.

Physical activity

The goal for physical activity focuses on maintaining healthy
body weight. The recommendation is for a total of one hour per day on most days
of the week of moderate-intensity activity, such as walking. This level of
physical activity is needed to maintain a healthy body weight, particularly for
people with sedentary occupations. The recommendation is based on calculations
of energy balance and on an analysis of the extensive literature on the
relationships between body weight and physical activity. This recommendation is
also presented elsewhere (21). Obviously, this quantitative goal cannot
be considered as a single best value by analogy with the nutrient
intake goals. Furthermore, it differs from the following widely accepted public
health recommendation (22):

For better health, people of all ages should
include a minimum of 30 minutes of physical activity of moderate intensity (such
as brisk walking) on most, if not all, days of the week. For most people greater
health benefits can be obtained by engaging in physical activity of more
vigorous intensity or of longer duration. This cardio respiratory endurance
activity should be supplemented with strength-developing exercises at least
twice a week for adults in order to improve musculo skeletal health, maintain
independence in performing the activities of daily life and reduce the risk of
falling.

The difference between the two recommendations results from
the difference in their focus. A recent symposium on the dose-response
relationships between physical activity and health outcomes found evidence that
30 minutes of moderate activity is sufficient for cardiovascular/metabolic
health, but not for all health benefits. Because prevention of obesity is a
central health goal, the recommendation of 60 minutes a day of
moderate-intensity activity is considered appropriate. Activity of moderate
intensity is found to be sufficient to have a preventive effect on most, if not
all, cardiovascular and metabolic diseases considered in this report. Higher
intensity activity has a greater effect on some, although not all, health
outcomes, but is beyond the capacity and motivation of a large majority of the
population.

Both recommendations include the idea that the daily activity
can be accomplished in several short bouts. It is important to point out that
both recommendations apply to people who are otherwise sedentary. Some
occupational activities and household chores constitute sufficient daily
physical exercise.

In recommending physical activity, potential individual risks
as well as benefits need to be assessed. In many regions of the world,
especially but not exclusively in rural areas of developing countries, an
appreciable proportion of the population is still engaged in physically
demanding activities relating to agricultural practices and domestic tasks
performed without mechanization or with rudimentary tools. Even children may be
required to undertake physically demanding tasks at very young ages, such as
collecting water and firewood and caring for livestock. Similarly, the
inhabitants of poor urban areas may still be required to walk long distances to
their jobs, which are usually of a manual nature and often require a high
expenditure of energy. Clearly, the recommendation for extra physical activity
is not relevant for these sectors of the population.

References

1. World Cancer Research Fund. Food, nutrition and
the prevention of cancer: a global perspective. Washington, DC, American
Institute for Cancer Research, 1997.

21. Weight control and physical activity. Lyon,
International Agency for Research on Cancer, 2002 (IARC Handbooks of Cancer
Prevention, Vol. 6).

22. Physical activity and health: a report of the Surgeon
General. Atlanta, GA, US Department of Health and Human Services, Centers
for Disease Control and Prevention, National Center for Chronic Disease
Prevention and Health Promotion, 1996.

5.2 Recommendations for preventing
excess weight gain and obesity

5.2.1 Background

Almost all countries (high-income and low-income alike) are
experiencing an obesity epidemic, although with great variation between and
within countries. In low-income countries, obesity is more common in middle-aged
women, people of higher socioeconomic status and those living in urban
communities. In more affluent countries, obesity is not only common in the
middle-aged, but is becoming increasingly prevalent among younger adults and
children. Furthermore, it tends to be associated with lower socioeconomic
status, especially in women, and the urban-rural differences are diminished or
even reversed.

It has been estimated that the direct costs of obesity
accounted for 6.8% (or US$ 70 billion) of total health care costs, and physical
inactivity for a furtherUS$24 billion, in the United States in 1995. Although
direct costs in other industrialized countries are slightly lower, they still
consume a sizeable proportion of national health budgets (1). Indirect
costs, which are far greater than direct costs, include workdays lost, physician
visits, disability pensions and premature mortality. Intangible costs such as
impaired quality of life are also enormous. Because the risks of diabetes,
cardiovascular disease and hypertension rise continuously with increasing
weight, there is much overlap between the prevention of obesity and the
prevention of a variety of chronic diseases, especially type 2 diabetes.
Population education strategies will need a solid base of policy and
environment-based changes to be effective in eventually reversing these
trends.

5.2.2 Trends

The increasing industrialization, urbanization and
mechanization occurring in most countries around the world is associated with
changes in diet and behaviour, in particular, diets are becoming richer in
high-fat, high energy foods and lifestyles more sedentary. In many developing
countries undergoing economic transition, rising levels of obesity often coexist
in the same population (or even the same household) with chronic undernutrition.
Increases in obesity over the past 30 years have been paralleled by a dramatic
rise in the prevalence of diabetes (2).

5.2.3 Diet, physical activity and
excess weight gain and obesity

Mortality rates increase with increasing degrees of
overweight, as measured by BMI. As BMI increases, so too does the proportion of
people with one or more comorbid conditions. In one study in the USA (3),
over half (53%) of all deaths in women with a BMI>29 kg/m2 could
be directly attributed to their obesity. Eating behaviours that have been linked
to overweight and obesity include snacking/eating frequency, binge-eating
patterns, eating out, and (protectively) exclusive breastfeeding. Nutrient
factors under investigation include fat, carbohydrate type (including refined
carbohydrates such as sugar), the glycaemic index of foods, and fibre.
Environmental issues are clearly important, especially as many environments
become increasingly obesogenic (obesity-promoting).

Physical activity is an important determinant of body weight.
In addition, physical activity and physical fitness (which relates to the
ability to perform physical activity) are important modifiers of mortality and
morbidity related to overweight and obesity. There is firm evidence that
moderate to high fitness levels provide a substantially reduced risk of
cardiovascular disease and all-cause mortality and that these benefits apply to
all BMI levels. Furthermore, high fitness protects against mortality at all BMI
levels in men with diabetes. Low cardiovascular fitness is a serious and common
comorbidity of obesity, and a sizeable proportion of deaths in overweight and
obese populations are probably a result of low levels of cardio-respiratory
fitness rather than obesity per se. Fitness is, in turn, influenced strongly by
physical activity in addition to genetic factors. These relationships emphasize
the role of physical activity in the prevention of overweight and obesity,
independently of the effects of physical activity on body weight.

5.2.4 Strength of
evidence

Convincing etiological factors

Regular physical activity (protective) and sedentary
lifestyles (causative). There is convincing evidence that regular physical
activity is protective against unhealthy weight gain whereas sedentary
lifestyles, particularly sedentary occupations and inactive recreation such as
watching television, promote it. Most epidemiological studies show smaller risk
of weight gain, overweight and obesity among persons who currently engage
regularly in moderate to large amounts of physical activity (4). Studies
measuring physical activity at baseline and randomized trials of exercise
programmes show more mixed results, probably because of the low adherence to
long-term changes. Therefore, it is ongoing physical activity itself rather than
previous physical activity or enrolment in an exercise programme that is
protective against unhealthy weight gain. The recommendation for individuals to
accumulate at least 30 minutes of moderate-intensity physical activity on most
days is largely aimed at reducing cardiovascular diseases and overall mortality.
The amount needed to prevent unhealthy weight gain is uncertain but is probably
significantly greater than this. Preventing weight gain after substantial weight
loss probably requires about 60-90 minutes per day. Two meetings recommended by
consensus that about 45-60 minutes of moderate-intensity physical activity is
needed on most days or every day to prevent unhealthy weight gain (5, 6).
Studies aimed at reducing sedentary behaviours have focused primarily on
reducing television viewing in children. Reducing viewing times by about 30
minutes a day in children in the United States appears feasible and is
associated with reductions in BMI.

Table 7. Summary of strength of evidence on factors that
might promote or protect against weight gain and
obesitya

a Strength of evidence: the totality of
the evidence was taken into account. The World Cancer Research Fund schema was
taken as the starting point but was modified in the following manner: randomized
controlled trials were given prominence as the highest ranking study design
(randomized controlled trials were not a major source of cancer evidence);
associated evidence and expert opinion was also taken into account in relation
to environmental determinants (direct trials were usually not
available).

b Specific amounts will depend on the analytical
methodologies used to measure fibre.

c Energy-dense and micronutrient-poor foods tend to
be processed foods that are high in fat and/or sugars. Low energy-dense (or
energy-dilute) foods, such as fruit, legumes, vegetables and whole grain
cereals, are high in dietary fibre and water.

d Associated evidence and expert opinion
included.

A high dietary intake of non-starch polysaccharides
(NSP)/dietary fibre (protective). The nomenclature and definitions of NSP
(dietary fibre) have changed with time, and many of the available studies used
previous definitions, such as soluble and insoluble fibre. Nevertheless, two
recent reviews of randomized trials have concluded that the majority of studies
show that a high intake of NSP (dietary fibre) promotes weight loss.

Pereira & Ludwig (7) found that 12 out of 19 trials
showed beneficial objective effects (including weight loss). In their review of
11 studies of more than 4 weeks duration, involving ad libitum eating Howarth
Saltzman & Roberts (8) reported a mean weight loss of 1.9 kg over 3.8
months. There were no differences between fibre type or between fibre consumed
in food or as supplements.

High intake of energy-dense micronutrient-poor foods
(causative).

There is convincing evidence that a high intake of
energy-dense foods promotes weight gain. In high-income countries (and
increasingly in low income countries) these energy-dense foods are not only
highly processed (low NSP) but also micronutrient-poor, further diminishing
their nutritional value. Energy-dense foods tend to be high in fat (e.g. butter,
oils, fried foods), sugars or starch, while energy-dilute foods have a high
water content (e.g. fruits and vegetables). Several trials have covertly
manipulated the fat content and the energy density of diets, the results of
which support the view that so-called passive over consumption of
total energy occurs when the energy density of the diet is high and that this is
almost always the case in high-fat diets. A meta-analysis of 16 trials of ad
libitum high-fat versus low-fat diets of at least 2 months duration suggested
that a reduction in fat content by 10% corresponds to about a 1 MJ reduction in
energy intake and about 3 kg in body weight (9). At a population level, 3
kg equates to about one BMI unit or about a 5% difference in obesity prevalence.
However, it is difficult to blind such studies and other non-physiological
effects may influence these findings (10). While energy from fat is no
more fattening than the same amount of energy from carbohydrate or protein,
diets that are high in fat tend to be energy-dense. An important exception to
this is diets based predominantly on energy-dilute foods (e.g. vegetables,
legumes, fruits) but which have a reasonably high percentage of energy as fat
from added oils.

The effectiveness over the long term of most dietary
strategies for weight loss, including low-fat diets, remains uncertain unless
accompanied by changes in behaviour affecting physical activity and food habits.
These latter changes at a public health level require an environment supportive
of healthy food choices and an active life. High quality trials to address these
issues are urgently needed. A variety of popular weight-loss diets that restrict
food choices may result in reduced energy intake and short term weight loss in
individuals but most do not have trial evidence of long-term effectiveness and
nutritional adequacy and therefore cannot be recommended for
populations.

Probable etiological factors

Home and school environments that promote healthy food and
activity choices for children (protective). Despite the obvious importance
of the roles that parents and home environments play on childrens eating
and physical activity behaviours, there is very little hard evidence available
to support this view. It appears that access and exposure to a range of fruits
and vegetables in the home is important for the development of preferences for
these foods and that parental knowledge, attitudes and behaviours related to
healthy diet and physical activity are important in creating role models
(11). More data are available on the impact of the school environment on
nutrition knowledge, on eating patterns and physical activity at school, and on
sedentary behaviours at home. Some studies (12), but not all, have shown
an effect of school-based interventions on obesity prevention. While more
research is clearly needed to increase the evidence base in both these areas,
supportive home and school environments were rated as a probable etiological
influence on obesity.

Heavy marketing of fast-food outlets and energy-dense,
micronutrient-poor foods and beverages (causative). Part of the consistent,
strong relationships between television viewing and obesity in children may
relate to the food advertising to which they are exposed (13-15).
Fast-food restaurants, and foods and beverages that are usually classified under
the eat least category in dietary guidelines are among the most
heavily marketed products, especially on television. Young children are often
the target group for the advertising of these products because they have a
significant influence on the foods bought by parents (16). The huge
expenditure on marketing fast-foods and other eat least choices (US$
11 billion in the United States alone in 1997) was considered to be a key factor
in the increased consumption of food prepared outside the home in general and of
energy-dense, micronutrient-poor foods in particular. Young children are unable
to distinguish programme content from the persuasive intent of advertisements.
The evidence that the heavy marketing of these foods and beverages to young
children causes obesity is not unequivocal. Nevertheless, the Consultation
considered that there is sufficient indirect evidence to warrant this practice
being placed in the probable category and thus becoming a potential
target for interventions (15-18).

A high intake of sugars-sweetened beverages
(causative). Diets that are proportionally low in fat will be proportionally
higher in carbohydrate (including a variable amount of sugars) and are
associated with protection against unhealthy weight gain, although a high intake
of free sugars in beverages probably promotes weight gain. The physiological
effects of energy intake on satiation and satiety appear to be quite different
for energy in solid foods as opposed to energy in fluids. Possibly because of
reduced gastric distension and faster transit times, the energy contained in
fluids is less well detected by the body and subsequent food intake
is poorly adjusted to account for the energy taken in through beverages
(19). This is supported by data from cross-sectional, longitudinal, and
cross-over studies (20-22). The high and increasing consumption of
sugars-sweetened drinks by children in many countries is of serious concern. It
has been estimated that each additional can or glass of sugars-sweetened drink
that they consume every day increases the risk of becoming obese by 60%
(19). Most of the evidence relates to soda drinks but many fruit drinks
and cordials are equally energy-dense and may promote weight gain if drunk in
large quantities. Overall, the evidence implicating a high intake of
sugars-sweetened drinks in promoting weight gain was considered moderately
strong.

Adverse socioeconomic conditions, especially for women in
high-income countries (causative). Classically the pattern of the
progression of obesity through a population starts with middle-aged women in
high-income groups but as the epidemic progresses, obesity becomes more common
in people (especially women) in lower socioeconomic status groups. The
relationship may even be bi-directional, setting up a vicious cycle (i.e. lower
socioeconomic status promotes obesity, and obese people are more likely to end
up in groups with low socioeconomic status). The mechanisms by which
socioeconomic status influences food and activity patterns are probably multiple
and need elucidation. However, people living in circumstances of low
socioeconomic status may be more at the mercy of the obesogenic environment
because their eating and activity behaviours are more likely to be the
default choices on offer. The evidence for an effect of low
socioeconomic status on predisposing people to obesity is consistent (in higher
income countries) across a number of cross-sectional and longitudinal studies
(23), and was thus rated as a probable cause of increased
risk of obesity.

Breastfeeding (protective). Breastfeeding as a
protective factor against weight gain has been examined in at least 20 studies
involving nearly 40 000 subjects. Five studies (including the two largest) found
a protective effect, two found that breastfeeding predicted obesity, and the
remainder found no relationships. There are probably multiple effects of
confounding in these studies; however, the reduction in the risk of developing
obesity observed in the two largest studies was substantial (20-37%). Promoting
breastfeeding has many benefits, the prevention of childhood obesity probably
being one of them.

Possible etiological factors

Several other factors were defined as possible
protective or causative in the etiology of unhealthy weight gain.

Low-glycaemic foods have been proposed as a potential
protective factor against weight gain and there are some early studies that
support this hypothesis. More clinical trials are, however, needed to establish
the association with greater certainty.

Large portion sizes are a possible causative factor for
unhealthy weight gain (24). The marketing of supersize
portions, particularly in fast-food outlets, is now common practice in many
countries. There is some evidence that people poorly estimate portion sizes and
that subsequent energy compensation for a large meal is incomplete and therefore
is likely to lead to overconsumption.

In many countries, there has been a steady increase in the
proportion of food eaten that is prepared outside the home. In the United
States, the energy, total fat, saturated fat, cholesterol and sodium content of
foods prepared outside the home is significantly higher than that of
home-prepared food. People in the United States who tend to eat in restaurants
have a higher BMI than those who tend to eat at home (25).

Certain psychological parameters of eating patterns may
influence the risk of obesity. The flexible restraint pattern is
associated with lower risk of weight gain, whereas the rigid
restraint/periodic disinhibition pattern is associated with a higher
risk.

Several other factors were also considered but the evidence
was not thought to be strong enough to warrant defining them as protective or
causative. Studies have not shown consistent associations between alcohol intake
and obesity despite the high energy density of the nutrient (7 kcal/g). There
are probably many confounding factors that influence the association. While a
high eating frequency has been shown in some studies to have a negative
relationship with energy intake and weight gain, the types of foods readily
available as snack foods are often high in fat and a high consumption of foods
of this type might predispose people to weight gain. The evidence regarding the
impact of early nutrition on subsequent obesity is also mixed, with some studies
showing relationships for high and low birth weights.

5.2.5 General strategies for obesity
prevention

The prevention of obesity in infants and young children should
be considered of high priority. For infants and young children, the main
preventive strategies are:

- the promotion of exclusive
breastfeeding;

- avoiding the use of added sugars and starches when feeding
formula;

- instructing mothers to accept their childs ability to
regulate energy intake rather than feeding until the plate is empty;

Additional measures include modifying the environment to
enhance physical activity in schools and communities, creating more
opportunities for family interaction (e.g. eating family meals), limiting the
exposure of young children to heavy marketing practices of energy-dense,
micronutrient-poor foods, and providing the necessary information and skills to
make healthy food choices.

In developing countries, special attention should be given to
avoidance of overfeeding stunted population groups. Nutrition programmes
designed to control or prevent undernutrition need to assess stature in
combination with weight to prevent providing excess energy to children of low
weight-for-age but normal weight-for-height. In countries in economic
transition, as populations become more sedentary and able to access energy-dense
foods, there is a need to maintain the healthy components of traditional diets
(e.g. high intake of vegetables, fruits and NSP). Education provided to mothers
and low socioeconomic status communities that are food insecure should stress
that overweight and obesity do not represent good health.

Low-income groups globally and populations in countries in
economic transition often replace traditional micronutrient-rich foods by
heavily marketed, sugars-sweetened beverages (i.e. soft drinks) and energy-dense
fatty, salty and sugary foods. These trends, coupled with reduced physical
activity, are associated with the rising prevalence of obesity. Strategies are
needed to improve the quality of diets by increasing consumption of fruits and
vegetables, in addition to increasing physical activity, in order to stem the
epidemic of obesity and associated diseases.

5.2.6 Disease-specific
recommendations

Body mass index (BMI)

BMI can be used to estimate, albeit crudely, the prevalence of
overweight and obesity within a population and the risks associated with it. It
does not, however, account for the wide variations in obesity between different
individuals and populations. The classification of overweight and obesity,
according to BMI, is shown in Table 8.

Table 8. Classification of overweight in adults according
to BMIa

Classification

BMI (kg/m2)

Risk of comorbidities

Underweight

<18.5

Low (but risk of other clinical problems increased)

Normal range

18.5 - 24.9

Average

Overweight

³ 25.0

Pre-obese

25.0 - 29.9

Increased

Obese class I

30.0 - 34.9

Moderate

Obese class II

35.0 - 39.9

Severe

Obese class III

³40.0

Very severe

a These BMI values are age-independent
and the same for both sexes. However, BMI may not correspond to the same degree
of fatness in different populations due, in part, to differences in body
proportions. The table shows a simplistic relationship between BMI and the risk
of comorbidity, which can be affected by a range of factors, including the
nature and the risk of comorbidity, which can be affected by a range of factors,
including the nature of the diet, ethnic group and activity level. The risks
associated with increasing BMI are continuous and graded and begin at a BMI
below 25. The interpretation of BMI gradings in relation to risk may differ for
different populations. Both BMI and a measure of fat distribution (waist
circumference or waist: hip ratio (WHR)) are important in calculating the risk
of obesity comorbidities.

Source: reference 26.

In recent years, different ranges of BMI cut-off points for
overweight and obesity have been proposed, in particular for the Asia-Pacific
region (27). At present available data on which to base definitive
recommendations are sparse.[4] Nevertheless, the
consultation considered that, to achieve optimum health, the median BMI for the
adult population should be in the range 21-23 kg/m2, while the goal
for individuals should be to maintain BMI in the range 18.5-24.9
kg/m2.

Waist circumference

Waist circumference is a convenient and simple measure which
is unrelated to height, correlates closely with BMI and the ratio of
waist-to-hip circumference, and is an approximate index of intra-abdominal fat
mass and total body fat. Furthermore, changes in waist circumference reflect
changes in risk factors for cardiovascular disease and other forms of chronic
diseases, even though the risks seem to vary in different populations. There is
an increased risk of metabolic complications for men with a waist circumference
³ 102 cm, and women with a waist circumference
³ 88 cm.

Physical activity

A total of one hour per day of moderate-intensity activity,
such as walking on most days of the week, is probably needed to maintain a
healthy body weight, particularly for people with sedentary
occupations.[5]

Total energy intake

The fat and water content of foods are the main determinants
of the energy density of the diet. A lower consumption of energy-dense (i.e.
high-fat, high-sugars and high-starch) foods and energy-dense (i.e. high free
sugars) drinks contributes to a reduction in total energy intake. Conversely, a
higher intake of energy-dilute foods (i.e. vegetables and fruits) and foods high
in NSP (i.e. wholegrain cereals) contributes to a reduction in total energy
intake and an improvement in micronutrient intake. It should be noted, however,
that very active groups who have diets high in vegetables, legumes, fruits and
wholegrain cereals, may sustain a total fat intake of up to 35% without the risk
of unhealthy weight gain.

5. Weight control and physical activity. Lyon,
International Agency for Research on Cancer, 2002 (IARC Handbooks of Cancer
Prevention, Vol. 6).

6. Saris WHM. Dose-response of physical activity in the
treatment of obesity-How much is enough to prevent unhealthy weight gain.
Outcome of the First Mike Stock Conference. International Journal of
Obesity, 2002, 26(Suppl. 1):S108.

16. Borzekowski DL, Robinson TN. The 30-second effect:
an experiment revealing the impact of television commercials on food preferences
of preschoolers. Journal of the American Dietetic Association, 2001,
101:42-46.

27. WHO Regional Office for the Western
Pacific/International Association for the Study of Obesity/International Obesity
Task Force. The Asia-Pacific perspective: redefining obesity and its
treatment. Sydney, Health Communications Australia, 2000.

5.3 Recommendations for preventing
diabetes

5.3.1 Background

Type 2 diabetes, formerly known as non-insulin-dependent
diabetes (NIDDM), accounts for most cases of diabetes worldwide. Type 2 diabetes
develops when the production of insulin is insufficient to overcome the
underlying abnormality of increased resistance to its action. The early stages
of type 2 diabetes are characterized by overproduction of insulin. As the
disease progresses, process insulin levels may fall as a result of partial
failure of the insulin producing b cells of the
pancreas. Complications of type 2 diabetes include blindness, kidney failure,
foot ulceration which may lead to gangrene and subsequent amputation, and
appreciably increased risk of infections, coronary heart disease and stroke. The
enormous and escalating economic and social costs of type 2 diabetes make a
compelling case for attempts to reduce the risk of developing the condition as
well as for energetic management of the established disease (1,
2).

Lifestyle modification is the cornerstone of both treatment
and attempts to prevent type 2 diabetes (3). The changes required to
reduce the risk of developing type 2 diabetes at the population level are,
however, unlikely to be achieved without major environmental changes to
facilitate appropriate choices by individuals. Criteria for the diagnosis of
type 2 diabetes and for the earlier stages in the disease process - impaired
glucose tolerance and impaired fasting glucose - have recently been revised
(4, 5).

Type 1 diabetes, previously known as insulin-dependent
diabetes, occurs much less frequently and is associated with an absolute
deficiency of insulin, usually resulting from autoimmune destruction of the
b cells of the pancreas. Environmental as well as
genetic factors appear to be involved but there is no convincing evidence of a
role for lifestyle factors which can be modified to reduce the risk.

5.3.2 Trends

Although increases in both the prevalence and incidence of
type 2 diabetes have occurred globally, they have been especially dramatic in
societies in economic transition in much of the newly industrialized world and
in developing countries (1, 6-9). Worldwide, the number of cases of
diabetes is currently estimated to be around 150 million. This number is
predicted to double by 2025, with the greatest number of cases being expected in
China and India. These numbers may represent an underestimate and there are
likely to be many undiagnosed cases. Previously a disease of the middle-aged and
elderly, type 2 diabetes has recently escalated in all age groups and is now
being identified in younger and younger age groups, including adolescents and
children, especially in high-risk populations.

Age-adjusted mortality rates among people with diabetes are
1.5-2.5 times higher than in the general population (10). In Caucasian
populations, much of the excess mortality is attributable to cardiovascular
disease, especially coronary heart disease (11, 12); amongst Asian and
American Indian populations, renal disease is a major contributor (13,
14), whereas in some developing nations, infections are an important cause
of death (15). It is conceivable that the decline in mortality due to
coronary heart disease which has occurred in many affluent societies may be
halted or even reversed if rates of type 2 diabetes continue to increase. This
may occur if the coronary risk factors associated with diabetes increase to the
extent that the risk they mediate outweighs the benefit accrued from
improvements in conventional cardiovascular risk factors and the improved care
of patients with established cardiovascular disease (3).

5.3.3 Diet, physical activity and
diabetes

Type 2 diabetes results from an interaction between genetic
and environmental factors. The rapidly changing incidence rates, however,
suggest a particularly important role for the latter as well as a potential for
stemming the tide of the global epidemic of the disease. The most dramatic
increases in type 2 diabetes are occurring in societies in which there have been
major changes in the type of diet consumed, reductions in physical activity, and
increases in overweight and obesity. The diets concerned are typically
energy-dense, high in saturated fatty acids and depleted in NSP.

In all societies, overweight and obesity are associated with
an increased risk of type 2 diabetes, especially when the excess adiposity is
centrally distributed. Conventional (BMI) categories may not be an appropriate
means of determining the risk of developing type 2 diabetes in individuals of
all population groups because of ethnic differences in body composition and
because of the importance of the distribution of excess adiposity. While all
lifestyle-related and environmental factors which contribute to excess weight
gain may be regarded as contributing to type 2 diabetes, the evidence that
individual dietary factors have an effect which is independent of their obesity
promoting effect, is inconclusive. Evidence that saturated fatty acids increase
risk of type 2 diabetes and that NSP are protective is more convincing than the
evidence for several other nutrients which have been implicated. The presence of
maternal diabetes, including gestational diabetes and intrauterine growth
retardation, especially when associated with later rapid catch-up growth,
appears to increase the risk of subsequently developing diabetes.

5.3.4 Strength of
evidence

The association between excessive weight gain, central
adiposity and the development of type 2 diabetes is convincing. The association
has been repeatedly demonstrated in longitudinal studies in different
populations, with a striking gradient of risk apparent with increasing levels of
BMI, adult weight gain, waist circumference or waist-to-hip ratio. Indeed waist
circumference or waist-to-hip ratio (reflecting abdominal or visceral adiposity)
are more powerful determinants of subsequent risk of type 2 diabetes than BMI
(16-20). Central adiposity is also an important determinant of insulin
resistance, the underlying abnormality in most cases of type 2 diabetes
(20). Voluntary weight loss improves insulin sensitivity (21) and
in several randomized controlled trials has been shown to reduce the risk of
progression from impaired glucose tolerance to type 2 diabetes (22,
23).

Longitudinal studies have clearly indicated that increased
physical activity reduces the risk of developing type 2 diabetes regardless of
the degree of adiposity (24-26). Vigorous exercise (i.e. training to an
intensity of 80-90% of age-predicted maximum heart rate for at least 20 minutes,
at least five times per week) has the potential to substantially enhance insulin
sensitivity (21). The minimum intensity and duration of physical activity
required to improve insulin sensitivity has not been established.

Offspring of diabetic pregnancies (including gestational
diabetes) are often large and heavy at birth, tend to develop obesity in
childhood and are at high risk of developing type 2 diabetes at an early age
(27). Those born to mothers after they have developed diabetes have a
three-fold higher risk of developing diabetes than those born before
(28).

In human intervention studies, replacement of saturated by
unsaturated fatty acids leads to improved glucose tolerance (40, 41) and
enhanced insulin sensitivity (42). Long-chain polyunsaturated fatty acids
do not, however, appear to confer additional benefit over monounsaturated fatty
acids in intervention studies (42). Furthermore, when total fat intake is
high (greater than 37% of total energy), altering the quality of dietary fat
appears to have little effect (42), a finding which is not surprising
given that in observational studies a high intake of total fat has been shown to
predict development of impaired glucose tolerance and the progression of
impaired glucose tolerance to type 2 diabetes (29, 43). A high total fat
intake has also been associated with higher fasting insulin concentrations and a
lower insulin sensitivity index (44, 45).

Considered in aggregate these findings are deemed to indicate
a probable causal link between saturated fatty acids and type 2 diabetes, and a
possible causal association between total fat intake and type 2 diabetes. The
two randomized controlled trials which showed a potential for lifestyle
modification to reduce the risk of progression from impaired glucose tolerance
to type 2 diabetes included advice to reduce total and saturated fat (22,
23), but in both trials it is impossible to disentangle the effects of
individual dietary manipulation.

Research relating to the association between NSP intake and
type 2 diabetes is complicated by ambiguity with regard to the definitions used
(the term dietary fibre and NSP are often incorrectly used interchangeably),
different methods of analysis and, consequently, inconsistencies in food
composition tables. Observations by Trowell in Uganda more than 30 years ago
suggested that the infrequency of diabetes in rural Africa may be the result of
a protective effect of substantial amounts of NSP in the diet (referred to as
dietary fibre) associated with a high consumption of minimally-processed or
unprocessed carbohydrate. The author also hypothesized that throughout the
world, increasing intakes of highly-processed carbohydrate, depleted in NSP, had
promoted the development of diabetes (46). Three cohort studies (the
Health Professionals Follow-up Study of men aged 40-75 years, the Nurses
Health Study of women aged 40-65 years, and the Iowa Womens Health Study
in women aged 55-69 years) have shown a protective effect of NSP (dietary fibre)
(47-49) which was independent of age, BMI, smoking and physical activity.
In many controlled experimental studies, high intakes of NSP (dietary fibre)
have repeatedly been shown to result in reduced blood glucose and insulin levels
in people with type 2 diabetes and impaired glucose tolerance (50).
Moreover an increased intake of wholegrain cereals, vegetables and fruits (all
rich in NSP) was a feature of the diets associated with a reduced risk of
progression of impaired glucose tolerance to type 2 diabetes in the two
randomized controlled trials previously described (22, 23). Thus the
evidence for a potential protective effect of NSP (dietary fibre) appears
strong. However, the fact that the experimental studies suggest that soluble
forms of NSP exert benefit (50-53) whereas the prospective cohort studies
suggest that it is the cereal-derived insoluble forms that are protective
(47, 48) explain the probable rather convincing
grading of the level of evidence.

Many foods which are rich in NSP (especially soluble forms),
such as pulses, have a low glycaemic index.[6]
Other carbohydrate-containing foods (e.g. certain types of pasta), which are not
especially high in NSP, also have a low glycaemic index. Low glycaemic index
foods, regardless of their NSP content, are not only associated with a reduced
glycaemic response after ingestion when compared with foods of higher glycaemic
index, but are also associated with an overall improvement in glycaemic control
(as measured by haemoglobin A1c) in people with diabetes (54-57). A low
glycaemic index does not, however, per se, confer overall health benefits, since
a high fat or fructose content of a food may also result in a reduced glycaemic
index and such foods may also be energy-dense. Thus while this property of
carbohydrate-containing foods may well influence the risk of developing type 2
diabetes, the evidence is accorded a lower level of strength than the evidence
relating to the NSP content. Similarly, the level of evidence for the protective
effect of n-3 fatty acids is regarded as possible because the
results of epidemiological studies are inconsistent and the experimental data
inconclusive. There is insufficient evidence to confirm or refute the
suggestions that chromium, magnesium, vitamin E and moderate intakes of alcohol
might protect against the development of type 2 diabetes.

A number of studies, mostly in developing countries, have
suggested that intrauterine growth retardation and low birth weight are
associated with subsequent development of insulin resistance (58). In
those countries where there has been chronic undernutrition, insulin resistance
may have been selectively advantageous in terms of surviving famine. In
populations where energy intake has increased and lifestyles have become more
sedentary, however, insulin resistance and the consequent risk of type 2
diabetes have been enhanced. In particular, rapid postnatal catch-up growth
appears to further increase the risk of type 2 diabetes in later life.
Appropriate strategies which may help to reduce type 2 diabetes risk in this
situation include improving the nutrition of young children, promoting linear
growth and preventing energy excess by limiting intake of energy-dense foods,
controlling the quality of fat supply, and facilitating physical activity. At a
population level, fetal growth may remain restricted until maternal height
improves. This may take several generations to correct. The prevention of type 2
diabetes in infants and young children may be facilitated by the promotion of
exclusive breastfeeding, avoiding overweight and obesity, and promoting optimum
linear growth. The strength of evidence on lifestyle factors is summarized in
Table 9.

b As a global public health recommendation, infants
should be exclusively breastfed for the first six months of life to achieve
optimal growth, development and health (59).

5.3.5 Disease-specific
recommendations

Measures aimed at reducing overweight and obesity, and
cardiovascular disease are likely to also reduce the risk of developing type 2
diabetes and its complications. Some measures are particularly relevant to
reducing the risk for diabetes; these are listed below:

Prevention/treatment of overweight and obesity, particularly in highrisk
groups.

Maintaining an optimum BMI,
i.e. at the lower end of the normal range. For the adult population, this means
maintaining a mean BMI in the range 21-23 kg/m2 and avoiding weight
gain (>5 kg) in adult life.

Voluntary weight reduction in
overweight or obese individuals with impaired glucose tolerance (although
screening for such individuals may not be cost-effective in many
countries).

Practising an endurance
activity at moderate or greater level of intensity (e.g. brisk walking) for one
hour or more per day on most days per week.

Ensuring that saturated fat
intake does not exceed 10% of total energy and for high-risk groups, fat intake
should be <7% of total energy.

4. Report of the Expert Committee on the Diagnosis and
Classification of Diabetes Mellitus. Diabetes Care, 1997,
20:1183-1197.

5. Definition, diagnosis and classification of diabetes
mellitus and its complications. Report of a WHO Consultation. Part 1. Diagnosis
and classification of diabetes mellitus. Geneva, World Health Organization,
1999 (document WHO/NCD/NCS/99.2).

40. Uusitupa M et al. Effects of two high-fat diets
with different fatty acid compositions on glucose and lipid metabolism in
healthy young women. American Journal of Clinical Nutrition, 1994,
59:1310-1316.

41. Vessby B et al. Substituting polyunsaturated for
saturated fat as a single change in a Swedish diet: effects on serum lipoprotein
metabolism and glucose tolerance in patients with hyperlipoproteinaemia.
European Journal of Clinical Investigation, 1980,
10:193-202.

5.4 Recommendations for preventing
cardiovascular diseases

5.4.1 Background

The second half of the 20th century has witnessed major shifts
in the pattern of disease, in addition to marked improvements in life
expectancy, this period is characterized by profound changes in diet and
lifestyles which in turn have contributed to an epidemic of noncommunicable
diseases. This epidemic is now emerging, and even accelerating, in most
developing countries, while infections and nutritional deficiencies are receding
as leading contributors to death and disability (1).

In developing countries, the effect of the nutrition
transition and the concomitant rise in the prevalence of cardiovascular diseases
will be to widen the mismatch between health care needs and resources, and
already scarce resources will be stretched ever more thinly. Because unbalanced
diets, obesity and physical inactivity all contribute to heart disease,
addressing these, along with tobacco use, can help to stem the epidemic. A large
measure of success in this area has already been demonstrated in many
industrialized countries.

5.4.2 Trends

Cardiovascular diseases are the major contributor to the
global burden of disease among the noncommunicable diseases. WHO currently
attributes one-third of all global deaths (15.3 million) to CVD, with developing
countries, low-income and middle-income countries accounting for 86% of the
DALYs lost to CVD world wide in 1998. In the next two decades the increasing
burden of CVD will be borne mostly by developing countries.

5.4.3 Diet, physical activity and
cardiovascular disease

The lag-time effect of risk factors for CVD means
that present mortality rates are the consequence of previous exposure to
behavioural risk factors such as inappropriate nutrition, insufficient physical
activity and increased tobacco consumption. Overweight, central obesity, high
blood pressure, dyslipidaemia, diabetes and low cardio-respiratory fitness are
among the biological factors contributing principally to increased risk.
Unhealthy dietary practices include the high consumption of saturated fats, salt
and refined carbohydrates, as well as low consumption of fruits and vegetables,
and these tend to cluster together.

5.4.4 Strength of
evidence

Convincing associations for reduced risk of CVD include
consumption of fruits (including berries) and vegetables, fish and fish oils
(eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), foods high in
linoleic acid and potassium, as well as physical activity and low to moderate
alcohol intake. While vitamin E intake appears to have no relationship to risk
of CVD, there is convincing evidence that myristic and palmitic acids, trans
fatty acids, high sodium intake, overweight and high alcohol intake contribute
to an increase in risk. A probable level of evidence demonstrates a
decreased risk for a-linolenic acid, oleic acid,
NSP, wholegrain cereals, nuts (unsalted), folate, plant sterols and stanols, and
no relationship for stearic acid. There is a probable increase in risk from
dietary cholesterol and unfiltered boiled coffee. Possible associations for
reduced risk include intake of flavonoids and consumption of soy products, while
possible associations for increased risk include fats rich in lauric acid, b-carotene supplements and impaired fetal nutrition. The
evidence supporting these conclusions is summarized below.

Fatty acids and dietary cholesterol

The relationship between dietary fats and CVD, especially
coronary heart disease, has been extensively investigated, with strong and
consistent associations emerging from a wide body of evidence accrued from
animal experiments, as well as observational studies, clinical trials and
metabolic studies conducted in diverse human populations (2).

Saturated fatty acids raise total and low-density lipoprotein
(LDL) cholesterol, but individual fatty acids within this group, have different
effects (3-5). Myristic and palmitic acids have the greatest effect and
are abundant in diets rich in dairy products and meat. Stearic acid has not been
shown to elevate blood cholesterol and is rapidly converted to oleic acid in
vivo. The most effective replacement for saturated fatty acids in terms of
coronary heart disease outcome are polyunsaturated fatty acids, especially
linoleic acid. This finding is supported by the results of several large
randomized clinical trials, in which replacement of saturated and trans fatty
acids by polyunsaturated vegetable oils lowered coronary heart disease risk
(6).

Trans fatty acids are geometrical isomers of cis-unsaturated
fatty acids that adapt a saturated fatty acid-like configuration. Partial
hydrogenation, the process used to increase shelf-life of polyunsaturated fatty
acids (PUFAs) creates trans fatty acids and also removes the critical double
bonds in essential fatty acids necessary for the action. Metabolic studies have
demonstrated that trans fatty acids render the plasma lipid profile even more
atherogenic than saturated fatty acids, by not only elevating LDL cholesterol to
similar levels but also by decreasing highdensity lipoprotein (HDL) cholesterol
(7). Several large cohort studies have found that intake of trans fatty
acids increases the risk of coronary heart disease (8, 9). Most trans
fatty acids are contributed by industrially hardened oils. Even though trans
fatty acids have been reduced or eliminated from retail fats and spreads in many
parts of the world, deep-fried fast foods and baked goods are a major and
increasing source (7).

When substituted for saturated fatty acids in metabolic
studies, both monounsaturated fatty acids and n-6 polyunsaturated fatty acids
lower plasma total and LDL cholesterol concentrations (10); PUFAs are
somewhat more effective than monounsaturates in this respect. The only
nutritionally important monounsaturated fatty acids is oleic acid, which is
abundant in olive and canola oils and also in nuts. The most important
polyunsaturated fatty acid is linoleic acid, which is abundant especially in
soybean and sunflower oils. The most important n-3 PUFAs are eicosapentaenoic
acid and docosahexaenoic acid found in fatty fish, and a-linolenic acid found in plant foods. The biological
effects of n-3 PUFAs are wide ranging, involving lipids and lipoproteins, blood
pressure, cardiac function, arterial compliance, endothelial function, vascular
reactivity and cardiac electrophysiology, as well as potent antiplatelet and
anti-inflammatory effects (11). The very long chain n-3 PUFAs
(eicosapentaenoic acid and docosahexaenoic acid) powerfully lower serum
triglycerides but they raise serum LDL cholesterol. Therefore, their effect on
coronary heart disease is probably mediated through pathways other than serum
cholesterol.

Most of the epidemiological evidence related to n-3 PUFAs is
derived from studies of fish consumption in populations or interventions
involving fish diets in clinical trials (evidence on fish consumption is
discussed further below). Fish oils have been used in the Gruppo Italiano per lo
Studio della Sopravvivenza nellInfarto Miocardico (GISSI) trial involving
survivors of myocardial infarction (12). After 3.5 years of follow-up,
the group that received fish oil had a 20% reduction in total mortality, a 30%
reduction in cardiovascular death and a 45% decrease in sudden death. Several
prospective studies have found an inverse association between the intake of
a-linolenic acid, (high in flaxseed, canola and
soybean oils), and risk of fatal coronary heart disease (13,
14).

Cholesterol in the blood and tissues is derived from two
sources: diet and endogenous synthesis. Dairy fat and meat are major dietary
sources. Egg yolk is particularly rich in cholesterol but unlike dairy products
and meat does not provide saturated fatty acids. Although dietary cholesterol
raises plasma cholesterol levels (15), observational evidence for an
association of dietary cholesterol intake with CVD is contradictory (16).
There is no requirement for dietary cholesterol and it is advisable to keep the
intake as low as possible (2). If intake of dairy fat and meat are
controlled, there is no need to severely restrict egg yolk intake, although some
limitation remains prudent.

Dietary plant sterols, especially sitostanol, reduce serum
cholesterol by inhibiting cholesterol absorption (17). The
cholesterol-lowering effects of plant sterols has also been well documented
(18) and commercial products made of these compounds are widely
available, but their longterm effects remain to be seen.

NSP (dietary fibre)

Dietary fibre is a heterogeneous mixture of polysaccharides
and lignin that cannot be degraded by the endogenous enzymes of vertebrate
animals. Water-soluble fibres include pectins, gums, mucilages and some
hemicelluloses. Insoluble fibres include cellulose and other hemicelluloses.
Most fibres reduce plasma total and LDL cholesterol, as reported by several
trials (19). Several large cohort studies carried out in different
countries have reported that a high fibre diet as well as a diet high in
wholegrain cereals lowers the risk of coronary heart disease
(20-23).

Antioxidants, folate, and flavonoids

Even though antioxidants could, in theory, be protective
against CVD and there is observational data supporting this theory, controlled
trials employing supplements have been disappointing. The Heart Outcomes
Prevention Evaluation trial (HOPE), a definitive clinical trial relating vitamin
E supplementation to CVD outcomes, revealed no effect of vitamin E
supplementation on myocardial infarction, stroke or death from cardiovascular
causes in men or women(24). Also, the results of the Heart Protection
Study indicated that no significant benefits of daily supplementation of vitamin
E, vitamin C and b-carotene were observed among the
high-risk individuals that were the subject of the study (25). In several
studies where dietary vitamin C reduced the risk of coronary heart disease,
supplemental vitamin C had little effect. Clinical trial evidence is lacking at
present. Observational cohort studies have suggested a protective role for
carotenoids but a meta-analysis of four randomized trials, in contrast, reported
an increased risk of cardiovascular death (26).

The relationship of folate to CVD has been mostly explored
through its effect on homocysteine, which may itself be an independent risk
factor for coronary heart disease and probably also for stroke. Folic acid is
required for the methylation of homocysteine to methionine. Reduced plasma
folate has been strongly associated with elevated plasma homocysteine levels and
folate supplementation has been demonstrated to decrease those levels
(27). However, the role of homocysteine as an independent risk factor for
CVD has been subject to much debate, since several prospective studies have not
found this association to be independent of other risk factors (28, 29).
It has also been suggested that elevation of plasma homocysteine is a
consequence and not a cause of atherosclerosis, wherein impaired renal function
resulting from atherosclerosis raises plasma homocysteine levels (30,
31). Data from the Nurses Health Study showed that folate and vitamin
B6, from diet and supplements, conferred protection against coronary heart
disease (32). A recently published metaanalysis concluded that a higher
intake of folate (0.8 mg folic acid) would reduce the risk of ischaemic heart
disease by 16% and stroke by 24% (33).

Flavonoids are polyphenolic compounds that occur in a variety
of foods of vegetable origin, such as tea, onions and apples. Data from several
prospective studies indicate an inverse association of dietary flavonoids with
coronary heart disease (34, 35). However, confounding may be a major
problem and may explain the conflicting results of observational
studies.

Sodium and potassium

High blood pressure is a major risk factor for coronary heart
disease and both forms of stroke (ischaemic and haemorrhagic). Of the many risk
factors associated with high blood pressure, the dietary exposure that has been
most investigated is daily sodium intake. It has been studied extensively in
animal experimental models, in epidemiological studies, controlled clinical
trials and in population studies on restricted sodium intake (36,
37).

All these data show convincingly that sodium intake is
directly associated with blood pressure. An overview of observational data
obtained from population studies suggested that a difference in sodium intake of
100 mmol per day was associated with average differences in systolic blood
pressure of 5 mmHg at age 15-19 years and 10 mmHg at age 60-69 years
(37). Diastolic blood pressures are reduced by about half as much, but
the association increases with age and magnitude of the initial blood pressure.
It was estimated that a universal reduction in dietary intake of sodium by 50
mmol per day would lead to a 50% reduction in the number of people requiring
antihypertensive therapy, a 22% reduction in the number of deaths resulting from
strokes and a16%reduction in the number of deaths from coronary heart disease.
The first prospective study using 24-hour urine collections for measuring sodium
intake, which is the only reliable measure, demonstrated a positive relationship
between an increased risk of acute coronary events, but not stroke events, and
increased sodium excretion (38). The association was strongest among
overweight men.

Several clinical intervention trials, conducted to evaluate
the effects of dietary salt reduction on blood pressure levels, have been
systematically reviewed (39, 40). Based on an overview of 32
methodologically adequate trials, Cutler, Follmann & Allender (39)
concluded that a daily reduction of sodium intake by 70-80 mmol was associated
with a lowering of blood pressure both in hypertensive and normotensive
individuals, with systolic and diastolic blood pressure reductions of 4.8/1.9
mmHg in the former and 2.5/1.1 mmHg in the latter. Clinical trials have also
demonstrated the sustainable blood pressure lowering effects of sodium
restriction in infancy (41, 42), as well as in the elderly in whom it
provides a useful nonpharmacological therapy (43). The results of a
low-sodium diet trial (44) showed that low-sodium diets, with 24-hour
sodium excretion levels around 70 mmol, are effective and safe. Two population
studies, in China and in Portugal, have also revealed significant reductions in
blood pressure in the intervention groups (45, 46).

A meta-analysis of randomized controlled trials showed that
potassium supplements reduced mean blood pressures (systolic/diastolic) by
1.8/1.0 mmHg in normotensive subjects and 4.4/2.5 mmHg in hypertensive subjects
(47). Several large cohort studies have found an inverse association
between potassium intake and risk of stroke (48, 49). While potassium
supplements have been shown to have protective effects on blood pressure and
cardiovascular diseases, there is no evidence to suggest that long-term
potassium supplements should be administered to reduce the risk for CVD. The
recommended levels of fruit and vegetable consumption assure an adequate intake
of potassium.

Food items and food groups

While the consumption of fruits and vegetables has been widely
believed to promote good health, evidence related to their protective effect
against CVD has only been presented in recent years (50). Numerous
ecological and prospective studies have reported a significant protective
association for coronary heart disease and stroke with consumption of fruits and
vegetables (50-53). The effects of increased fruit and vegetable
consumption on blood pressure alone and in combination with a low-fat diet, were
assessed in the Dietary Approaches to Stop Hypertension (DASH) trial
(54). While the combination diet was more effective in lowering blood
pressure, the fruit and vegetable diet also lowered blood pressure (by 2.8 mmHg
systolic and 1.1 mmHg diastolic) in comparison to the control diet. Such
reductions, while seeming modest at the individual level, would result in a
substantial reduction in population-wide risk of CVD by shifting the blood
pressure distribution.

Most, but not all, population studies have shown that fish
consumption is associated with a reduced risk of coronary heart disease. A
systematic review concluded that the discrepancy in the findings may be a result
of differences in the populations studied, with only high-risk individuals
benefiting from increasing their fish consumption (55). It was estimated
that in high-risk populations, an optimum fish consumption of 40-60 g per day
would lead to approximately a 50% reduction in death from coronary heart
disease. In a diet and reinfarction trial, 2-year mortality was reduced by 29%
in survivors of a first myocardial infarction in persons receiving advice to
consume fatty fish at least twice a week (56). A recent study based on
data from 36 countries, reported that fish consumption is associated with a
reduced risk of death from all causes as well as CVD mortality
(57).

Several large epidemiological studies have demonstrated that
frequent consumption of nuts was associated with decreased risk of coronary
heart disease (58, 59). Most of these studies considered nuts as a group,
combining many different types of nuts. Nuts are high in unsaturated fatty acids
and low in saturated fats, and contribute to cholesterol lowering by altering
the fatty acid profile of the diet as a whole. However, because of the high
energy content of nuts, advice to include them in the diet must be tempered in
accordance with the desired energy balance.

Several trials indicate that soy has a beneficial effect on
plasma lipids (60, 61). A composite analysis of 38 clinical trials found
that an average consumption of 47 g of soy protein a day led to a 9% decline in
total cholesterol and a 13% decline in LDL cholesterol in subjects free of
coronary heart disease (62). Soy is rich in isoflavones, compounds that
are structurally and functionally similar to estrogen. Several animal
experiments suggest that the intake of these isoflavones may provide protection
against coronary heart disease, but human data on efficacy and safety are still
awaited.

There is convincing evidence that low to moderate alcohol
consumption lowers the risk of coronary heart disease. In a systematic review of
ecological, case-control and cohort studies in which specific associations were
available between risk of coronary heart-disease and consumption of beer, wine
and spirits, it was found that all alcoholic drinks are linked with lower risk
(63). However, other cardiovascular and health risks associated with
alcohol do not favour a general recommendation for its use.

Boiled, unfiltered coffee raises total and LDL cholesterol
because coffee beans contain a terpenoid lipid called cafestol. The amount of
cafestol in the cup depends on the brewing method: it is zero for paper-filtered
drip coffee, and high in the unfiltered coffee still widely drunk in, for
example, in Greece, the Middle East and Turkey. Intake of large amounts of
unfiltered coffee markedly raises serum cholesterol and has been associated with
coronary heart disease in Norway (64). A shift from unfiltered, boiled
coffee to filtered coffee has contributed significantly to the decline in serum
cholesterol in Finland (65).

5.4.5 Disease-specific
recommendations

Measures aimed at reducing the risk of CVD are outlined below.
The strength of evidence on lifestyle factors is summarized in Table
10.

Fats

Dietary intake of fats strongly influences the risk of
cardiovascular diseases such as coronary heart disease and stroke, through
effects on blood lipids, thrombosis, blood pressure, arterial (endothelial)
function, arrythmogenesis and inflammation. However, the qualitative composition
of fats in the diet has a significant role to play in modifying this
risk.

Table 10. Summary of strength of evidence on lifestyle
factors and risk of developing cardiovascular diseases

The evidence shows that intake of saturated fatty acids is
directly related to cardiovascular risk. The traditional target is to restrict
the intake of saturated fatty acids to less than 10%, of daily energy intake and
less than 7% for high-risk groups. If populations are consuming less than 10%,
they should not increase that level of intake. Within these limits, intake of
foods rich in myristic and palmitic acids should be replaced by fats with a
lower content of these particular fatty acids. In developing countries, however,
where energy intake for some population groups may be inadequate, energy
expenditure is high and body fat stores are low (BMI <18.5 kg/m2). The amount
and quality of fat supply has to be considered keeping in mind the need to meet
energy requirements. Specific sources of saturated fat, such as coconut and palm
oil, provide low-cost energy and may be an important source of energy for the
poor.

Not all saturated fats have similar metabolic effects; those
with 12-16 carbons in the fatty acid chain have a greater effect on raising LDL
cholesterol. This implies that the fatty acid composition of the fat source
should be examined. As populations progress in the nutrition transition and
energy excess becomes a potential problem, restricting certain fatty acids
becomes progressively more relevant to ensuring cardiovascular health.

To promote cardiovascular health, diets should provide a very
low intake of trans fatty acids (hydrogenated oils and fats). In practice, this
implies an intake of less than 1% of daily energy intake. This recommendation is
especially relevant in developing countries where low-cost hydrogenated fat is
frequently consumed. The potential effect of human consumption of hydrogenated
oils of unknown physiological effects (e.g. marine oils) is of great
concern.

Diets should provide an adequate intake of PUFAs, i.e. in the
range 6-10% of daily energy intake. There should also be an optimal balance
between intake of n-6 PUFAs and n-3 PUFAs, i.e. 5-8% and 1-2% of daily energy
intake, respectively.

Intake of oleic acid, a monounsaturated fatty acid, should
make up the rest of the daily energy intake from fats, to give a daily total fat
intake ranging from15%up to30%of daily energy intake. Recommendations for total
fat intake may be based on current levels of population consumption in different
regions and modified to take account of age, activity and ideal body weight.
Where obesity is prevalent, for example, an intake in the lower part of the
range is preferable in order to achieve a lower energy intake. While there is no
evidence to directly link the quantity of daily fat intake to an increased risk
of CVD, total fat consumption should be limited to enable the goals of reduced
intake of saturated and trans fatty acids to be met easily in most populations
and to avoid the potential problems of undesirable weight gain that may arise
from unrestricted fat intake. It should be noted that highly active groups with
diets rich in vegetables, legumes, fruits and wholegrain cereals will limit the
risk of unhealthy weight gain on a diet comprising a total fat intake of up to
35%.

These dietary goals can be met by limiting the intake of fat
from dairy and meat sources, avoiding the use of hydrogenated oils and fats in
cooking and manufacture of food products, using appropriate edible vegetable
oils in small amounts, and ensuring a regular intake of fish (one to two times
per week) or plant sources of a-linolenic acid.
Preference should be given to food preparation practices that employ non-frying
methods.

Fruits and vegetables

Fruits and vegetables contribute to cardiovascular health
through the variety of phytonutrients, potassium and fibre that they contain.
Daily intake of fresh fruit and vegetables (including berries, green leafy and
cruciferous vegetables and legumes), in an adequate quantity (400-500 g per
day), is recommended to reduce the risk of coronary heart disease, stroke and
high blood pressure.

Sodium

Dietary intake of sodium, from all sources, influences blood
pressure levels in populations and should be limited so as to reduce the risk of
coronary heart disease and both forms of stroke. Current evidence suggests that
an intake of no more than 70 mmol or 1.7 g of sodium per day is beneficial in
reducing blood pressure. The special situation of individuals (i.e. pregnant
women and non-acclimated people who perform strenuous physical activity in hot
environments) who may be adversely affected by sodium reduction needs to be kept
in mind.

Limitation of dietary sodium intake to meet these goals should
be achieved by restricting daily salt (sodium chloride) intake to less than 5 g
per day. This should take into account total sodium intake from all dietary
sources, for example additives such as monosodium glutamate and preservatives.
Use of potassium-enriched low-sodium substitutes is one way to reduce sodium
intake. The need to adjust salt iodization, depending on observed sodium intake
and surveillance of iodine status of the population, should be
recognized.

Potassium

Adequate dietary intake of potassium lowers blood pressure and
is protective against stroke and cardiac arrythmias. Potassium intake should be
at a level which will keep the sodium to potassium ratio close to 1.0, i.e. a
daily potassium intake level of 70-80 mmol per day. This may be achieved through
adequate daily consumption of fruits and vegetables.

Fibre is protective against coronary heart disease and has
also been used in diets to lower blood pressure. Adequate intake may be achieved
through fruits, vegetables and wholegrain cereals.

Fish

Regular fish consumption (1-2 servings per week) is protective
against coronary heart disease and ischaemic stroke and is recommended. The
serving should provide an equivalent of 200-500 mg of eicosapentaenoic and
docosahexaenoic acid. People who are vegetarians are recommended to ensure
adequate intake of plant sources of a-linolenic
acid.

Alcohol

Although regular low to moderate consumption of alcohol is
protective against coronary heart disease, other cardiovascular and health risks
associated with alcohol do not favour a general recommendation for its
use.

Physical activity

Physical activity is related to the risk of cardiovascular
diseases, especially coronary heart disease, in a consistent inverse
dose-response fashion when either volume or intensity are used for assessment.
These relationships apply to both incidence and mortality rates from all
cardiovascular diseases and from coronary heart disease. At present, no
consistent dose-response relationship can be found between risk of stroke and
physical activity. The lower limits of volume or intensity of the protective
dose of physical activity have not been defined with certainty, but the current
recommendation of at least 30 minutes of at least moderate-intensity physical
activity on most days of the week is considered sufficient. A higher volume or
intensity of activity would confer a greater protective effect. The recommended
amount of physical activity is sufficient to raise cardiorespiratory fitness to
the level that has been shown to be related to decreased risk of cardiovascular
disease. Individuals who are unaccustomed to regular exercise or have a
high-risk profile for CVD should avoid sudden and high-intensity bursts of
physical activity.

43. Whelton PK et al. Sodium reduction and weight loss
in the treatment of hypertension in older persons. Journal of the American
Medical Association, 1998, 279:839-846 (erratum appears in Journal
of the American Medical Association, 1998, 279:1954).

5.5 Recommendations for preventing
cancer

5.5.1 Background

Cancer is caused by a variety of identified and unidentified
factors. The most important established cause of cancer is tobacco smoking.
Other important determinants of cancer risk include diet, alcohol and physical
activity, infections, hormonal factors and radiation. The relative importance of
cancers as a cause of death is increasing, mostly because of the increasing
proportion of people who are old, and also in part because of reductions in
mortality from some other causes, especially infectious diseases. The incidence
of cancers of the lung, colon and rectum, breast and prostate generally
increases in parallel with economic development, while the incidence of stomach
cancer usually declines with development.

5.5.2 Trends

Cancer is now a major cause of mortality throughout the world
and, in the developed world, is generally exceeded only by cardiovascular
diseases. An estimated 10 million new cases and over 6 million deaths from
cancer occurred in 2000 (1). As developing countries become urbanized,
patterns of cancer, including those most strongly associated with diet, tend to
shift towards those of economically developed countries. Between 2000 and 2020,
the total number of cases of cancer in the developing world is predicted to
increase by 73% and, in the developed world, to increase by 29%, largely as a
result of an increase in the number of old people (1).

5.5.3 Diet, physical activity and
cancer

Dietary factors are estimated to account for approximately 30%
of cancers in industrialized countries (2), making diet second only to
tobacco as a theoretically preventable cause of cancer. This proportion is
thought to be about 20% in developing countries (3), but may grow with
dietary change, particularly if the importance of other causes, especially
infections, declines. Cancer rates change as populations move between countries
and adopt different dietary (and other) behaviours, further implicating dietary
factors in the etiology of cancer.

Body weight and physical inactivity together are estimated to
account for approximately one-fifth to one-third of several of the most common
cancers, specifically cancers of the breast (postmenopausal), colon,
endometrium, kidney and oesophagus (adenocarcinoma) (4).

5.5.4 Strength of
evidence

Research to date has uncovered few definite relationships
between diet and cancer risk. Dietary factors for which there is convincing
evidence for an increase in risk are overweight and obesity, and a high
consumption of alcoholic beverages, aflatoxins, and some forms of salting and
fermenting fish. There is also convincing evidence to indicate that physical
activity decreases the risk of colon cancer. Factors which probably increase
risk include high dietary intake of preserved meats, salt-preserved foods and
salt, and very hot (thermally) drinks and food. Probable protective factors are
consumption of fruits and vegetables, and physical activity (for breast cancer).
After tobacco, overweight and obesity appear to be the most important known
avoidable causes of cancer.

The role of diet in the etiology of the major
cancers

Cancers of the oral cavity, pharynx and oesophagus. In
developed countries the main risk factors for cancers of the oral cavity,
pharynx and oesophagus are alcohol and tobacco, and up to 75% of such cancers
are attributable to these two lifestyle factors (5). Overweight and
obesity are established risk factors specifically for adenocarcinoma (but not
squamous cell carcinoma) of the oesophagus (6-8). In developing
countries, around 60% of cancers of the oral cavity, pharynx and oesophagus are
thought to be a result of micronutrient deficiencies related to a restricted
diet that is low in fruits and vegetables and animal products (5, 9). The
relative roles of various micronutrients are not yet clear (5, 9). There
is also consistent evidence that consuming drinks and foods at a very high
temperature increases the risk for these cancers (10). Nasopharyngeal
cancer is particularly common in South-East Asia (11), and has been
clearly associated with a high intake of Chinese-style salted fish, especially
during early childhood (12, 13), as well as with infection with the
Epstein-Barr virus (2).

Stomach cancer. Until about 20 years ago stomach cancer
was the most common cancer in the world, but mortality rates have been falling
in all industrialized countries (14) and stomach cancer is currently much
more common in Asia than in North America or Europe (11). Infection with
the bacterium Helicobacter pylori is an established risk factor, but not
a sufficient cause, for the development of stomach cancer (15). Diet is
thought to be important in the etiology of this disease; substantial evidence
suggests that risk is increased by high intakes of some traditionally preserved
salted foods, especially meats and pickles, and with salt per se, and that risk
is decreased by high intakes of fruits and vegetables (16), perhaps
because of their vitamin C content. Further prospective data are needed, in
particular to examine whether some of the dietary associations may be partly
confounded by Helicobacter pylori infection and whether dietary factors
may modify the association of Helicobacter pylori with risk.

Colorectal cancer. Colorectal cancer incidence rates
are approximately ten-fold higher in developed than in developing countries
(11), and it has been suggested that diet-related factors mayaccount for
up to80%of the differences in rates between countries (17). The best
established diet-related risk factor is overweight/obesity (8) and
physical activity has been consistently associated with a reduced risk of colon
cancer (but not of rectal cancer) (8, 18). These factors together,
however, do not explain the large variation between populations in colorectal
cancer rates. There is almost universal agreement that some aspects of the
westernized diet are a major determinant of risk; for instance,
there is some evidence that risk is increased by high intakes of meat and fat,
and that risk is decreased by high intakes of fruits and vegetables, dietary
fibre, folate and calcium, but none of these hypotheses has been firmly
established.

International correlation studies have shown a strong
association between per capita consumption of meat and colorectal cancer
mortality (19), and a recent systematic review concluded that preserved
meat is associated with an increased risk for colorectal cancer but that fresh
meat is not (20). However, most studies have not observed positive
associations with poultry or fish (9). Overall, the evidence suggests
that high consumption of preserved and red meat probably increases the risk for
colorectal cancer.

As with meat, international correlation studies show a strong
association between per capita consumption of fat and colorectal cancer
mortality (19). However, the results of observational studies of fat and
colorectal cancer have, overall, not been supportive of an association with fat
intake (9, 21).

Many case-control studies have observed a weak association
between the risk of colorectal cancer and high consumption of fruits and
vegetables and/or dietary fibre (22, 23), but the results of recent large
prospective studies have been inconsistent (24-26). Furthermore, results
from randomized controlled trials have not shown that intervention over a 3-4
year period with supplemental fibre or a diet low in fat and high in fibre and
fruits and vegetables can reduce the recurrence of colorectal adenomas
(27-29). It is possible that some of the inconsistencies are a result of
differences between studies in the types of fibre eaten and in the methods for
classifying fibre in food tables, or that the association with fruits and
vegetables arises principally from an increase in risk at very low levels of
consumption (30). On balance, the evidence that is currently available
suggests that intake of fruits and vegetables probably reduces the risk for
colorectal cancer.

Recent studies have suggested that vitamins and minerals might
influence the risk for colorectal cancer. Some prospective studies have
suggested that a high intake of folate from diet or vitamin supplements is
associated with a reduced risk for colon cancer (31-33). Another
promising hypothesis is that relatively high intakes of calcium may reduce the
risk for colorectal cancer; several observational studies have supported this
hypothesis (9, 34), and two trials have indicated that supplemental
calcium may have a modest protective effect on the recurrence of colorectal
adenomas (29, 35).

Liver cancer. Approximately 75% of cases of liver
cancer occur in developing countries, and liver cancer rates vary over 20-fold
between countries, being much higher in sub-Saharan Africa and South-East Asia
than in North America and Europe (11). The major risk factor for
hepatocellular carcinoma, the main type of liver cancer, is chronic infection
with hepatitis B, and to a lesser extent, hepatitis C virus (36).
Ingestion of foods contaminated with the mycotoxin, aflatoxin is an important
risk factor among people in developing countries, together with active hepatitis
virus infection (13, 37). Excessive alcohol consumption is the main
diet-related risk factor for liver cancer in industrialized countries, probably
via the development of cirrhosis and alcoholic hepatitis (5).

Pancreatic cancer. Cancer of the pancreas is more
common in industrialized countries than in developing countries (11, 38).
Overweight and obesity possibly increase the risk (9, 39). Some studies
have suggested that risk is increased by high intakes of meat, and reduced by
high intakes of vegetables, but these data are not consistent
(9).

Lung cancer. Lung cancer is the most common cancer in
the world (11). Heavy smoking increases the risk by around 30-fold, and
smoking causes over 80% of lung cancers in developed countries (5).
Numerous observational studies have found that lung cancer patients typically
report a lower intake of fruits, vegetables and related nutrients (such as b-carotene) than controls (9, 34). The only one of
these factors to have been tested in controlled trials, namely b-carotene, has, however, failed to produce any benefit
when given as a supplement for up to 12 years (40-42). The possible
effect of diet on lung cancer risk remains controversial, and the apparent
protective effect of fruits and vegetables may be largely the result of residual
confounding by smoking, since smokers generally consume less fruit and
vegetables than non-smokers. In public health terms, the overriding priority for
preventing lung cancer is to reduce the prevalence of smoking.

Breast cancer. Breast cancer is the second most common
cancer in the world and the most common cancer among women. Incidence rates are
about five times higher in industrialized countries than in less developed
countries and Japan (11). Much of this international variation is a
result of differences in established reproductive risk factors such as age at
menarche, parity and age at births, and breastfeeding (43, 44), but
differences in dietary habits and physical activity may also contribute. In
fact, age at menarche is partly determined by dietary factors, in that
restricted dietary intake during childhood and adolescence leads to delayed
menarche. Adult height, also, is weakly positively associated with risk, and is
partly determined by dietary factors during childhood and adolescence
(43). Estradiol and perhaps other hormones play a key role in the
etiology of breast cancer (43), and it is possible that any further
dietary effects on risk are mediated by hormonal mechanisms.

The only dietary factors which have been shown to increase the
risk for breast cancer are obesity and alcohol. Obesity increases breast cancer
risk in postmenopausal women by around 50%, probably by increasing serum
concentrations of free estradiol (43). Obesity does not increase risk
among premenopausal women, but obesity in premenopausal women is likely to lead
to obesity throughout life and therefore to an eventual increase in breast
cancer risk. For alcohol, there is now a large body of data from well-designed
studies which consistently shows a small increase in risk with increasing
consumption, with about a 10% increase in risk for an average of one alcoholic
drink every day (45). The mechanism for this association is not known,
but may involve increases in estrogen levels (46).

The results of studies of other dietary factors including fat,
meat, dairy products, fruits and vegetables, fibre and phyto-estrogens are
inconclusive (9, 34, 47, 48).

Endometrial cancer. Endometrial cancer risk is about
three-fold higher in obese women than in lean women (8, 49), probably
because of the effects of obesity on hormone levels (50). Some
case-control studies have suggested that diets high in fruits and vegetables may
reduce risk and that diets high in saturated or total fat may increase risk, but
the amount of available data is limited (9).

Prostate cancer. Prostate cancer incidence rates are
strongly affected by diagnostic practices and therefore difficult to interpret,
but mortality rates show that death from prostate cancer is about 10 times more
common in North America and Europe than in Asia (11).

Little is known about the etiology of prostate cancer,
although ecological studies suggest that it is positively associated with a
westernized diet (19). The data from prospective studies have
not established causal or protective associations for specific nutrients or
dietary factors (9, 34). Diets high in red meat, dairy products and
animal fat have frequently been implicated in the development of prostate
cancer, although the data are not entirely consistent (9, 51-53).
Randomized controlled trials have provided substantial, consistent evidence that
supplements of b-carotene do not alter the risk for
prostate cancer (40, 41, 54) but have suggested that vitamin E
(54) and selenium (55) might have a protective effect. Lycopene,
primarily from tomatoes, has been associated with a reduced risk in some
observational studies, but the data are not consistent (56). Hormones
control the growth of the prostate, and diet might influence prostate cancer
risk by affecting hormone levels.

Kidney cancer. Overweight and obesity are established
risk factors for cancer of the kidney, and may account for up to 30% of kidney
cancers in both men and women (57).

Table 11 provides a summary of strength of evidence with
regard to the role of various risk factors in the development of
cancer.

Table 11. Summary of strength of evidence on lifestyle
factors and the risk of developing cancer

a The convincing and
probable categories in this report correspond to the
sufficient category of the IARC report on weight control and
physical activity (4) in terms of the public health and policy
implications.

b For colorectal cancer, a protective effect of
fruit and vegetable intake has been suggested by many case-control studies but
this has not been supported by results of several large prospective studies,
suggesting that if a benefit does exist it is likely to be modest.

The Consultation recognized the problems posed by the lack of
data on diet and cancer from the developing world. There are very limited data
from Africa, Asia and Latin America, yet these regions represent two-thirds or
more of the world population. There is thus an urgent need for epidemiological
research on diet and cancer in these regions. The need to evaluate the role of
food processing methods, traditional and industrial, was also identified.
Microbiological and chemical food contaminants may also contribute to
carcinogenicity of diets.

The nutrition transition is accompanied by changes in
prevalence of specific cancers. For some cancers, such as stomach cancer, this
may be beneficial while for others, such as colorectal and breast cancers, the
changes are adverse.

5.5.5 Disease-specific
recommendations

The main recommendations for reducing the risk of developing
cancer are as follows:

Maintain weight
(among adults) such that BMI is in the range of 18.5-24.9 kg/m2 and avoid weight
gain (>5 kg) during adult life (58).

Maintain regular physical
activity. The primary goal should be to perform physical activity on most days
of the week; 60 minutes per day of moderate-intensity activity, such as walking,
may be needed to maintain healthy body weight in otherwise sedentary people.
More vigorous activity, such as fast walking, may give some additional benefits
for cancer prevention (4).

Consumption of alcoholic
beverages is not recommended: if consumed, do not exceed two
units[8] per day.

Chinese-style fermented salted
fish should only be consumed in moderation, especially during childhood. Overall
consumption of salt-preserved foods and salt should be moderate.

Minimize exposure to aflatoxin
in foods.

Have a diet which includes at
least 400 g per day of total fruits and vegetables.

Those who are not vegetarian
are advised to moderate consumption of preserved meat (e.g. sausages, salami,
bacon, ham).[9]

Do not consume foods or drinks
when they are at a very hot (scalding hot) temperature.

13. Some naturally occurring substances: food items and
constituents, heterocyclic aromatic amines and mycotoxins. Lyon,
International Agency for Research on Cancer, 1993 (IARC Monographs on the
Evaluation of Carcinogenic Risks to Humans, Vol. 56).

14. World health statistics annual. Geneva, World
Health Organization, 2001 (available on the Internet at
http://www.who.int/whosis/).

19. Armstrong B, Doll R. Environmental factors and
cancer incidence and mortality in different countries, with special reference to
dietary practices. International Journal of Cancer, 1975,
15:617-631.

34. Nutritional Aspects of the Development of Cancer.
Report of the Working Group on Diet and Cancer of the Committee on Medical
Aspects of Food and Nutrition Policy. London, The Stationery Office, 1998
(Report on Health and Social Subjects, No. 48).

40. Hennekens CH et al. Lack of effect of long-term
supplementation with betacarotene on the incidence of malignant neoplasms and
cardiovascular disease. New England Journal of Medicine, 1996,
334:1145-1149.

41. Omenn GS et al. Effects of a combination of beta
carotene and vitamin A on lung cancer and cardiovascular disease. New England
Journal of Medicine, 1996, 334:1150-1155.

42. Beta Carotene Cancer Prevention Study Group The
Alpha-Tocopherol. The effect of vitamin E and beta carotene on the incidence
of lung cancer and other cancers in male smokers. New England Journal of
Medicine, 1994, 330:1029-1035.

54. Heinonen OP et al. Prostate cancer and
supplementation with alpha-tocopherol and beta-carotene: incidence and mortality
in a controlled trial. Journal of the National Cancer Institute, 1998,
90:440-446.

5.6 Recommendations for preventing
dental diseases

5.6.1 Background

Oral health is related to diet in many ways, for example,
through nutritional influences on cranio-facial development, oral cancer and
oral infectious diseases. The purpose of this review, however, is to focus on
the nutritional aspects of dental diseases. Dental diseases include dental
caries, developmental defects of enamel, dental erosion and periodontal disease.
Dental diseases are a costly burden to health care services, accounting for
between 5% and 10% of total health care expenditures and exceeding the cost of
treating cardiovascular disease, cancer and osteoporosis in industrialized
countries (1). In low-income countries, the cost of traditional
restorative treatment of dental disease would probably exceed the available
resources for health care. Dental health promotion and preventive strategies are
clearly more affordable and sustainable.

Although not life-threatening, dental diseases have a
detrimental effect on quality of life in childhood through to old age, having an
impact on self-esteem, eating ability, nutrition and health. In modern society,
a significant role of teeth is to enhance appearance; facial appearance is very
important in determining an individuals integration into society, and
teeth also play an essential role in speech and communication. Oral diseases are
associated with considerable pain, anxiety and impaired social functioning
(2, 3). Dental decay may result in tooth loss, which reduces the ability
to eat a nutritious diet, the enjoyment of food, the confidence to socialize and
the quality of life (4-6).

5.6.2 Trends

The amount of dental decay is measured using the dmf/DMF
index, a count of the number of teeth or surfaces in a persons mouth that
are decayed, missing or filled as a result of caries in primary dentition/
permanent dentition. An additional dental status indicator is the proportion of
the population who are edentulous (have no natural teeth).

In most low-income countries, the prevalence rate of dental
caries is relatively low and more than 90% of caries are untreated. Available
data (7) show that the mean number of decayed, missing or filled
permanent teeth (DMFT) at age 12 years in low-income countries is 1.9, 3.3 in
middle-income countries and 2.1 in high-income countries (Table 12).

Data on the level of dental caries in the permanent dentition
of 12-yearolds show two distinct trends. First, a fall in the prevalence of
dental caries in developed countries, and second an increase in the prevalence
of the disease in some developing countries that have increased their
consumption of sugars and have not yet been introduced to the presence of
adequate amounts of fluoride. Despite the marked overall decline in dental
caries over the past 30 years, the prevalence of dental caries remains
unacceptably high in many developed countries. Even in countries with low
average DMFT scores, a significant proportion of children have relatively high
levels of dental caries. Moreover, there is some indication that the favourable
trends in levels of dental caries in permanent teeth have come to a halt
(8).

Many developing countries have low decayed, missing, filled
primary teeth (dmft) values but a high prevalence of dental caries in the
primary dentition. Data on 5-year-old children in Europe suggest that the trend
towards reduced prevalence of dental decay has halted (9-11). In children
aged 5-7 years, average dmft values of below 2.0 have been reported for Denmark,
England, Finland, Italy, Netherlands and Norway (12). Higher dmft values
were reported recently for Belarus (4.7) (13), Hungary (4.5) (14),
Romania (4.3) (15) and the Russian Federation (4.7)
(16).

Being free from caries at age 12 years does not imply being
caries-free for life. The mean DMFT in countries of the European Union after
1988 varied between 13.4 and 20.8 at 35-44 years (17). The WHO guidelines
on oral health state that at age 35-44 years a DMFT score of 14 or above
is considered high. In most developing countries, the level of caries in adults
of this age group is lower, for example, 2.1 in China (18) and 5.7 in
Niger (19). Few data are available on the prevalence and severity of root
caries in older adults, but with the increasingly ageing population and greater
retention of teeth, the problem of root caries is likely to become a significant
public health concern in the future.

The number of edentulous persons has declined over the past
20-30 years in several industrialized countries (3). Despite overall
gains however, there is still a large proportion of older adults who are
edentulous or partially dentate and as the population continues to age tooth
loss will affect a growing number of persons worldwide. Table 13 summarizes the
available information on the prevalence of edentulousness in old-age populations
throughout the world.

Dental erosion is a relatively new dental problem in many
countries throughout the world, and is related to diet. There is anecdotal
evidence that prevalence is increasing in industrialized countries, but there
are no data over time to indicate patterns of this disease. There are
insufficient data available to comment on worldwide trends; in some populations,
however, it is thought that approximately50%of children are affected
(20).

5.6.3 Diet and dental
disease

Nutritional status affects the teeth pre-eruptively, although
this influence is much less important than the post-eruptive local effect of
diet on the teeth (21). Deficiencies of vitamins D and A and
protein-energy malnutrition have been associated with enamel hypoplasia and
salivary gland atrophy (which reduces the mouths ability to buffer plaque
acids), which render the teeth more susceptible to decay. In developing
countries, in the absence of dietary sugars, undernutrition is not associated
with dental caries. Undernutrition coupled with a high intake of sugars may
exacerbate the risk of caries.

There is some evidence to suggest that periodontal disease
progresses more rapidly in undernourished populations (22); the important
role of nutrition in maintaining an adequate host immune response may explain
this observation. Apart from severe vitamin C deficiency, which may result in
scurvy-related periodontitis, there is little evidence at present for an
association between diet and periodontal disease. Current research is
investigating the potential role of the antioxidant nutrients in periodontal
disease. Poor oral hygiene is the most important risk factor in the development
of periodontal disease (21). Undernutrition exacerbates the severity of
oral infections (e.g. acute necrotizing ulcerative gingivitis) and may
eventually lead to their evolution into life-threatening diseases such as noma,
a dehumanizing oro-facial gangrene (23).

Table 13. Prevalence of edentulousness in older people
throughout the world

Country or area

Prevalence of edentulousness (%)

Age group (years)

African Region

Gambia

6

65 +

Madagascar

25

65-74

Region of the Americas

Canada

58

65 +

United Sates

26

65-69

South-East Asian Region

India

19

65-74

Indonesia

24

65 +

Sri Lanka

37

65-74

Thailand

16

65 +

European Region

Albania

69

65 +

Austria

15

65-74

Bosnia and Herzegovina

78

65 +

Bulgaria

53

65 +

Denmark

27

65-74

Finland

41

65 +

Hungary

27

65-74

Iceland

15

65-74

Italy

19

65-74

Lithuania

14

65-74

Poland

25

65-74

Romania

26

65-74

Slovakia

44

65-74

Slovenia

16

65 +

United Kingdom

46

65 +

Eastern Mediterranean Region

Egypt

7

65 +

Lebanon

20

64-75

Saudi Arabia

31-46

65 +

Western Pacific Region

Cambodia

13

65-74

China

11

65-74

Malaysia

57

65 +

Singapore

21

65 +

Source: reference 7.

Dental caries occur because of demineralization of enamel and
dentine by organic acids formed by bacteria in dental plaque through the
anaerobic metabolism of sugars derived from the diet (24). Organic acids
increase the solubility of calcium hydroxyapatite in the dental hard tissues and
demineralization occurs. Saliva is super-saturated with calcium and phosphate at
pH 7 which promotes remineralization. If the oral pH remains high enough for
sufficient time then complete remineralization of enamel may occur. If the acid
challenge is too great, however, demineralization dominates and the enamel
becomes more porous until finally a carious lesion forms (25). The
development of caries requires the presence of sugars and bacteria, but is
influenced by the susceptibility of the tooth, the bacterial profile, and the
quantity and quality of the saliva.

Dietary sugars and dental caries

There is a wealth of evidence from many different types of
investigation, including human studies, animal experiments and experimental
studies in vivo and in vitro to show the role of dietary sugars in the etiology
of dental caries (21). Collectively, data from these studies provide an
overall picture of the cariogenic potential of carbohydrates. Sugars are
undoubtedly the most important dietary factor in the development of dental
caries. Here, the term sugars refers to all monosaccharides and
disaccharides, while the term sugar refers only to sucrose. The term
free sugars refers to all monosaccharides and disaccharides added to
foods by the manufacturer, cook or consumer, plus sugars naturally present in
honey, fruit juices and syrups. The term fermentable carbohydrate
refers to free sugars, glucose polymers, oligosaccharides and highly refined
starches; it excludes non-starch polysaccharides and raw starches.

Worldwide epidemiological studies have compared sugar
consumption and levels of dental caries at the between-country level. Sreebny
(26, 27) correlated the dental caries experience (DMFT) of 12-year-olds
with data on sugar supplies of 47 countries and found a significant correlation
(+0.7); 52% of the variation in the level of caries was explained by the per
capita availability of sugar. In countries with a consumption level of sugar
<18 kg per person per year caries experience was consistently <DMFT3. A
later analysis by Woodward & Walker (28) did not find a similar
association for developed countries. Sugar availability nevertheless accounted
for 28% of the variation in levels of dental caries; 23 out of 26 countries with
a per capita sugar availability <50g per day had a mean DMFT score for
12-year olds of <3, whereas only half of the countries with sugar
availability above this level had achieved a DMFT score that was<3.

Miyazaki & Morimoto (29) reported a significant
correlation (r = +0.91) between sugar availability in Japan and DMFT at
age 12 years between 1957 and 1987. Populations that had experienced a reduced
sugar availability during the Second World War showed a reduction in dental
caries which subsequently increased again when the restriction was lifted
(30-32). Although the data pre-date the widespread use of fluoride
dentifrice, Weaver (33) observed a reduction in dental caries between
1943 and 1949 in areas of northern England with both high and low concentrations
of fluoride in drinking-water.

Isolated communities with a traditional way of life and a
consistently low intake of sugars have very low levels of dental caries. As
economic levels in such societies rise, the amount of sugar and other
fermentable carbohydrates in the diet increases and this is often associated
with a marked increase in dental caries. Examples of this trend have been
reported among the Inuit in Alaska, USA (34), as well as in populations
in Ethiopia (35), Ghana (36), Nigeria (37), Sudan
(38), and on the Island of Tristan da Cunha, St Helena
(39).

There is evidence to show that many groups of people with high
exposure to sugars have levels of caries higher than the population average.
Examples include children with chronic diseases requiring long-term
sugar-containing medicines (40), and confectionery workers
(41-44). Likewise, experience of dental caries has seldom been reported
in groups of people who have a habitually low intake of sugars, for example,
children of dentists (45, 46) and children in institutions where strict
dietary regimens are inflicted (47, 48). A weakness of population studies
of this type is that changes in intake of sugars often occur concurrently with
changes in the intake of refined starches, making it impossible to attribute
changes in dental caries solely to changes in the intake of sugars. An exception
to this are the data from studies of children with hereditary fructose
intolerance (HFI). Studies have shown that people with HFI have a low intake of
sugars and a higher than average intake of starch, but have a low dental caries
experience (49).

Human intervention studies are rare, and those that have been
reported are now decades old and were conducted in the pre-fluoride era before
the strong link between sugars intake and dental caries levels was established.
It would not be possible to repeat such studies today because of ethical
constraints. The Vipeholm study, conducted in an adult mental institution in
Sweden between 1945 and 1953 (50), investigated the effects of consuming
sugary foods of varying stickiness and at different times throughout the day on
the development of caries. It was found that sugar, even when consumed in large
amounts, had little effect on caries increment if it was ingested up to a
maximum of four times a day at mealtimes only. Increased frequency of
consumption of sugar between meals was, however, associated with a marked
increase in dental caries. It was also found that the increase in dental caries
activity disappears on withdrawal of sugar-rich foods. Despite the complicated
nature of the study the conclusions are valid, although they apply to the
pre-fluoride era. The Turku study was a controlled dietary intervention study
carried out on adults in Finland in the 1970s which showed that almost total
substitution of sucrose in the diet with xylitol (a non-cariogenic sweetener)
resulted in an 85% reduction in dental caries over a 2-year period
(51).

Numerous cross-sectional epidemiological studies have compared
sugars intake with dental caries levels in many countries of the world. Those
conducted before the early 1990s have been summarized by Rugg-Gunn (21).
Nine out of 21 studies that compared amount of sugars consumed with caries
increment found significant associations, while the other 12 did not. Moreover,
23 out of 37 studies that investigated the association between frequency of
sugars consumption and caries levels found significant relationships, while 14
failed to find any such associations.

A cross-sectional study in the United States of 2514 people
aged 9-29 years conducted between 1968 and 1970 found that the dental caries
experience of adolescents eating the highest amounts of sugars (upper 15% of the
sample) was twice that of those eating the lowest amounts (lower 15% of the
sample) (52). Granath et al. (53) showed that intake of sugars was
the most important factor associated with caries in the primary dentition of
preschool children in Sweden. When the effects of oral hygiene and fluoride were
kept constant, the children with a low intake of sugars between meals had up to
86% less caries than those with high intakes of sugars. Other studies have found
fluoride exposure and oral hygiene to be more strongly associated with caries
than sugars consumption (54, 55). A recent study in the United Kingdom of
a representative sample of children aged 4-18 years showed no significant
relationship between caries experience and level of intake of free sugars; in
the age group 15-18 years, however, the upper band of free sugars consumers were
more likely to have decay than the lower band (70% compared with 52%)
(20).

Many other cross-sectional studies have shown a relationship
between sugars consumption and levels of caries in the primary and/or permanent
dentitions in countries or areas throughout the world, including China
(56), Denmark (57), Madagascar (58, 59), Saudi Arabia
(60), Sweden (61, 62), Thailand (63) and the United Kingdom
(64).

When investigating the association between diet and the
development of dental caries it is more appropriate to use a longitudinal study
design in which sugars consumption habits over time are related to changes in
dental caries experience. Such studies have shown a significant relationship
between caries development and sugars intake (65-67). In a comprehensive
study of over 400 children in England aged 11-12 years, a small but significant
relationship was found between intake of total sugars and caries increment over
2 years (r = +0.2) (67). The Michigan Study in the United States
investigated the relationship between sugars intake and dental caries increment
over 3 years in children initially aged 10-15 years (66). A weak
relationship was found between the amount of dietary sugars consumed and dental
caries experience.

In a review of longitudinal studies, Marthaler (68)
analysed the relationship between dietary sugars and caries activity in
countries where the availability of sugars is high and the use of fluoride is
extensive. He concluded that in modern societies that make use of prevention,
the relationship between sugars consumption and dental caries was still evident
(68). He also concluded that many older studies had failed to show a
relationship between sugars intake and development of dental caries because they
were of poor methodological design, used unsuitable methods of dietary analysis
or were of insufficient power (68). Correlations between
individuals sugars consumption and dental caries increments may be weak if
the range of sugars intake in the study population is small. That is to say,
that if all people within a population are exposed to the disease risk factor,
the relationship between the risk factor and the disease will not be apparent
(69).

Frequency and amount of sugars consumption. Several
studies, including the above-mentioned Vipeholm study in Sweden, have indicated
that caries experience increases markedly when the frequency of sugars intake
exceeds four times a day (50, 70-72). The importance of frequency versus
the total amount of sugars is difficult to evaluate as the two variables are
hard to distinguish from each other. Data from animal studies have indicated the
importance of frequency of sugars intake in the development of dental caries
(73, 74). Some human studies have also shown that the frequency of sugars
intake is an important etiological factor for caries development (75).
Many studies have related the frequency of intake of sugars or sugars-rich food
to caries development but have not simultaneously investigated the relationship
between amount of sugars consumed and dental caries, and therefore no conclusion
regarding the relative importance of these two variables can be drawn from these
studies (76-78).

Animal studies have also shown a relationship between amount
of sugars consumed and the development of dental caries (79-82). Several
longitudinal studies in humans have indicated that the amount of sugars consumed
is more important than the frequency (66, 67, 83, 84), while Jamel et al.
(85) found that both the frequency and the amount of sugars intake are
important.

The strong correlation between both the amount and frequency
of sugars consumption has been demonstrated by several investigators in
different countries (67, 86-88). It is therefore highly likely that, in
terms of caries development, both variables are potentially important.

Relative cariogenicity of different sugars and food
consistency. Therelative acidogenicity of different monosaccharides and
disaccharides has been investigated in plaque pH studies, which have shown that
lactose is less acidogenic than other sugars (89). Animal studies have
provided no clear evidence that, with the exception of lactose, the
cariogenicity of monosaccharides and disaccharides differs. The above-mentioned
study in Turku, Finland, found no difference in caries development between
subjects on diets sweetened with sucrose compared with those whose diet had been
sweetened with fructose (51). Invert sugar (50% fructose + 50% glucose)
is less cariogenic than sucrose (90).

The adhesiveness or stickiness of a food is not necessarily
related to either oral retention time or cariogenic potential. For example,
consumption of sugars-containing drinks (i.e. non-sticky) is associated with
increased risk of dental caries (85, 88)

Potential impact of sugars reduction on other dietary
components. It is important to consider the potential impact of a reduction
in free sugars on other components of the diet. Simple, cross-sectional analysis
of dietary data from populations has shown an inverse relationship between the
intake of free sugars and the intake of fat (91), suggesting that
reducing free sugars might lead to an increase in fat intake. There is, however,
a growing body of evidence from studies over time that shows that changes in
intake of fat and free sugars are not inversely related, and that reductions in
intake of fat are offset by increases in intakes of starch rather than free
sugars (92, 93). Cole-Hamilton et al. (94) found that the intake
of both fat and added sugars simultaneously decreased as fibre intake increased.
Overall dietary goals that promote increased intake of wholegrain staple foods,
fruits and vegetables and a reduced consumption of free sugars are thus unlikely
to lead to an increased consumption of fat.

Influence of fluoride. Fluoride undoubtedly protects
against dental caries (95). The inverse relationship between fluoride in
drinking-water and dental caries, for instance, is well established. Fluoride
reduces caries in children by between 20% and 40%, but does not eliminate dental
caries altogether.

Over 800 controlled trials of the effect of fluoride
administration on dental caries have been conducted; collectively these studies
demonstrate that fluoride is the most effective preventive agent against caries
(95). Several studies have that indicated that a relationship between
sugars intake and caries still exists in the presence of adequate fluoride
exposure (33, 71, 96, 97). In two major longitudinal studies in children,
the observed relationships between sugars intake and development of dental
caries remained even after controlling for use of fluoride and oral hygiene
practices (66, 67). As mentioned earlier, following a review of available
longitudinal studies, Marthaler (68) concluded that, even when preventive
measures such as use of fluoride are employed, a relationship between sugars
intake and caries still exists. He also stated that in industrialized countries
where there is adequate exposure to fluoride, no further reduction in the
prevalence and severity of dental caries will be achieved unless the intake of
sugars is reduced.

A recent systematic review that investigated the importance of
sugars intake in caries etiology in populations exposed to fluoride concluded
that where there is adequate exposure to fluoride, sugars consumption is a
moderate risk factor for caries in most people; moreover sugars consumption is
likely to be a more powerful indicator for risk of caries in persons who do not
have regular exposure to fluoride. Thus, restricting sugars consumption still
has a role to play in the prevention of caries in situations where there is
widespread use of fluoride but this role is not as strong as it is without
exposure to fluoride (98). Despite the indisputable preventive role of
fluoride, there is no strong evidence of a clear relationship between oral
cleanliness and levels of dental caries (99-100).

Excess ingestion of fluoride during enamel formation can lead
to dental fluorosis. This condition is observed particularly in countries that
have high levels of fluoride in water supplies (95).

Starches and dental caries

Epidemiological studies have shown that starch is of low risk
to dental caries. People who consume high-starch/low-sugars diets generally have
low levels of caries, whereas people who consume low-starch/highsugars diets
have high levels of caries (39, 48, 49, 51, 67, 101, 102). In Norway and
Japan the intake of starch increased during the Second World War, yet the
occurrence of caries was reduced.

The heterogeneous nature of starch (i.e. degree of refinement,
botanical origin, raw or cooked) is of particular relevance when assessing its
potential cariogenicity. Several types of experiment have shown that raw starch
is of low cariogenicity (103-105). Cooked starch is about onethird to
one-half as cariogenic as sucrose (106, 107). Mixtures of starch and
sucrose are, however, potentially more cariogenic than starch alone
(108). Plaque pH studies, using an indwelling oral electrode, have shown
starch-containing foods reduce plaque pH to below 5.5, but starches are less
acidogenic than sucrose. Plaque pH studies measure acid production from a
substrate rather than caries development, and take no account of the protective
factors found in some starch-containing foods or of the effect of foods on
stimulation of salivary flow.

Glucose polymers and pre-biotics are increasingly being added
to foods in industrialized countries. Evidence on the cariogenicity of these
carbohydrates is sparse and comes from animal studies, plaque pH studies and
studies in vitro which suggest that maltodextrins and glucose syrups are
cariogenic (109-111). Plaque pH studies and experiments in vitro suggest
that isomalto-oligosaccharides and gluco-oligosaccharides may be less acidogenic
than sucrose (112-114). There is, however, evidence that
fructo-oligosaccharides are as acidogenic as sucrose (115,
116).

Fruit and dental caries

As habitually consumed, there is little evidence to show that
fruit is an important factor in the development of dental caries (67,
117-119). A number of plaque pH studies have found fruit to be acidogenic,
although less so than sucrose (120-122). Animal studies have shown that
when fruit is consumed in very high frequencies (e.g. 17 times a day) it may
induce caries (123, 124), but less so than sucrose. In the only
epidemiological study in which an association between fruit consumption and DMFT
was found (125), fruit intakes were very high (e.g. 8 apples or 3 bunches
of grapes per day) and the higher DMFT in fruit farm workers compared with grain
farm workers arose solely from differences in the numbers of missing
teeth.

Dietary factors which protect against dental
caries

Some dietary components protect against dental caries. The
cariostatic nature of cheese has been demonstrated in several experimental
studies (126, 127), and in human observational studies (67) and
intervention studies (128). Cows milk contains calcium, phosphorus
and casein, all of which are thought to inhibit caries. Several studies have
shown that the fall in plaque pH following milk consumption is negligible
(129, 130). The cariostatic nature of milk has been demonstrated in
animal studies (131, 132). Rugg-Gunn et al. (67) found an inverse
relationship between the consumption of milk and caries increment in a study of
adolescents in England. Wholegrain foods have protective properties; they
require more mastication thereby stimulating increased saliva flow. Other foods
that are good gustatory and/or mechanical stimulants to salivary flow include
peanuts, hard cheeses and chewing gum. Both organic and inorganic phosphates
(found in unrefined plant foods) have been found to be cariostatic in animal
studies, but studies in humans have produced inconclusive results (133,
134). Both animal studies and experimental investigations in humans have
shown that black tea extract increases plaque fluoride concentration and reduces
the cariogenicity of a sugars-rich diet (135, 136).

Breastfeeding and dental caries

In line with the positive health effects of breastfeeding,
epidemiological studies have associated breastfeeding with low levels of dental
caries (137, 138). A few specific case studies have linked prolonged ad
libitum and nocturnal breastfeeding to early childhood caries. Breastfeeding has
the advantage that it does not necessitate the use of a feeder bottle, which has
been associated with early childhood caries. A breastfed infant will also
receive milk of a controlled composition to which additional free sugars have
not been added. There are no benefits to dental health of feeding using a
formula feed.

Dental erosion

Dental erosion is the progressive irreversible loss of dental
hard tissue that is chemically etched away from the tooth surface by extrinsic
and/or intrinsic acids by a process that does not involve bacteria. Extrinsic
dietary acids include citric acid, phosphoric acid, ascorbic acid, malic acid,
tartaric acid and carbonic acid found, for example, in fruits and fruit juices,
soft drinks and vinegar. Erosion in severe cases leads to total tooth
destruction (139). Human observational studies have shown an association
between dental erosion and the consumption of a number of acidic foods and
drinks, including frequent consumption of fruit juice, soft drinks (including
sports drinks), pickles (containing vinegar), citrus fruits and berries
(140-144). Age-related increases in dental erosion have been shown to be
greater in those with the highest intake of soft drinks (20).
Experimental clinical studies have shown that consumption of, or rinsing with,
acidic beverages significantly lowers the pH of the oral fluids (121).
Enamelis softened within one hour of exposure to cola but this may be reversed
by exposure to milk or cheese (145, 146). Animal studies have shown that
fruit and soft drinks cause erosion (124, 147), although fruit juices are
significantly more destructive than whole fruits (148, 149).

5.6.4 Strength of
evidence

The strength of the evidence linking dietary sugars to the
risk of dental caries is in the multiplicity of the studies rather than the
power of any individual study. Strong evidence is provided by the intervention
studies (50, 51) but the weakness of these studies is that they were
conducted in the pre-fluoride era. More recent studies also show an association
between sugars intake and dental caries albeit not as strong as in the
prefluoride era. However, in many developing countries people are not yet
exposed to the benefits of fluoride.

Cross-sectional studies should be interpreted with caution
because dental caries develop over time and therefore simultaneous measurements
of disease levels and diet may not give a true reflection of the role of diet in
the development of the disease. It is the diet several years earlier that may be
responsible for current caries levels. Longitudinal studies (66, 67) that
have monitored a change in caries experience and related this to dietary factors
provide stronger evidence. Such studies have been conducted on populations with
an overall high sugars intake but a low interindividual variation; this may
account for the weak associations that have been reported.

The studies that overcome the problem of low variation in
consumption of sugars are studies that have monitored dental caries following a
marked change in diet, for example, those conducted on populations during the
Second World War and studies of populations before and after the introduction of
sugars into the diet. Such studies have shown clearly that changes in dental
caries mirror changes in economic growth and increased consumption of free
sugars. Sometimes changes in sugars consumption were accompanied by an increase
in other refined carbohydrates. There are, however, examples where sugars
consumption decreased and starch consumption increased yet levels of dental
caries declined.

Strong evidence of the relationship between sugar availability
and dental caries levels comes from worldwide ecological studies (26,
28). The limitations of these studies are that they use data on sugar
availability and not actual intake, they do not measure frequency of sugars
intake, and they assume that level of intake is equal throughout the population.
Also, the values are for sucrose, yet many countries obtain a considerable
amount of their total sugars from other sugars. These studies have only
considered DMFT of 12-year-olds, not always from a representative sample of the
population.

Caution needs to be applied when extrapolating the results of
animal studies to humans because of differences in tooth morphology, plaque
bacterial ecology, salivary flow and composition, and the form in which the diet
is provided (usually powdered form in animal experiments). Nonetheless, animal
studies have enabled the effect on caries of defined types, frequencies and
amounts of carbohydrates to be studied.

Plaque pH studies measure plaque acid production, but the
acidogenicity of a foodstuff cannot be taken as a direct measurement of its
cariogenic potential. Plaque pH studies take no account of protective factors in
foods, salivary flow and the effects of other components of the diet. Many of
the plaque pH studies that show falls in pH below the critical value of 5.5 with
fruits and cooked starchy foods have been conducted using the indwelling
electrode technique. This electrode is recognized as being hypersensitive and
non-discriminating, tending to give an all or nothing response to
all carbohydrates (150).

Research has consistently shown that when annual sugar
consumption exceeds 15 kg per person per year (or 40 g per person per day)
dental caries increase with increasing sugar intake. When sugar consumption is
below 10 kg per person per year (around 27 g per person per day), levels of
dental caries are very low (26, 28, 29, 51, 151-158). Exposure to
fluoride (i.e. where the proportion of fluoride in drinking-water is 0.7-1.0
ppm, or where over 90% of toothpastes available contain fluoride) increases the
safe level of sugars consumption.

5.6.5 Disease-specific
recommendations

It is important to set a recommended maximum level for the
consumption of free sugars; a low free sugars consumption by a population will
translate into a low level of dental caries. Population goals enable the oral
health risks of populations to be assessed and health promotion goals
monitored.

The best available evidence indicates that the level of dental
caries is low in countries where the consumption of free sugars is below 15-20
kg per person per year. This is equivalent to a daily intake of 40-55 g per
person and the values equate to 6-10% of energy intake. It is of particular
importance that countries which currently have low consumption of free sugars
(<15-20 kg per person per year) do not increase consumption levels. For
countries with high consumption levels it is recommended that national health
authorities and decision-makers formulate countryspecific and community-specific
goals for reduction in the amount of free sugars, aiming towards the recommended
maximum of no more than 10% of energy intake.

In addition to population targets given in terms of the amount
of free sugars, targets for the frequency of free sugars consumption are also
important. The frequency of consumption of foods and/or drinks containing free
sugars should be limited to a maximum of four times per day.

Many countries that are currently undergoing nutrition
transition do not have adequate exposure to fluoride. There should be promotion
of adequate fluoride exposure via appropriate vehicles, for example, affordable
toothpaste, water, salt and milk. It is the responsibility of national health
authorities to ensure implementation of feasible fluoride programmes for their
country. Research into the outcome of alternative community fluoride programmes
should be encouraged.

In order to minimize the occurrence of dental erosion, the
amount and frequency of intake of soft drinks and juices should be limited.
Elimination of undernutrition prevents enamel hypoplasia and the other potential
effects of undernutrition on oral health (e.g. salivary gland atrophy,
periodontal disease, oral infectious diseases).

9. Pitts NB, Evans DJ. The dental caries experience of
5-year-old children in the United Kingdom. Surveys coordinated by the British
Association for the Study of Community Dentistry in 1995/96. Community Dental
Health, 1997, 14:47-52.

55. Hausen H, HeinonenOP, Paunio I. Modification of
occurrence of caries in children by toothbrushing and sugar exposure in
fluoridated and non-fluoridated area. Community Dentistry and Oral
Epidemiology, 1981, 9:103-107.

92. Alexy U, Sichert-Hellert W, Kersting M.
Fifteen-year time trends in energy and macronutrient intake in German
children and adolescents: results of the DONALD study. British Journal of
Nutrition, 2002, 87:595-604.

94. Cole-Hamilton I et al. A study among dietitians and
adult members of their households of the practicalities and implications of
following proposed dietary guidelines for the UK. British Dietetic Association
Community Nutrition Group Nutrition Guidelines Project. Human Nutrition -
Applied Nutrition, 1986, 40:365-389.

109. Grenby TH, Mistry M. Properties of maltodextrins
and glucose syrups in experiments in vitro and in the diets of laboratory
animals, relating to dental health. British Journal of Nutrition, 2000,
84:565-574.

118. Martinsson T. Socio-economic investigation of
school children with high and low caries frequency. 3. A dietary study based on
information given by the children. Odontologisk Revy, 1972,
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119. Savara BS, Suher T. Dental caries in children one
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158. Knowles EM. The effects of enemy occupation on the
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1946:161-172.

5.7 Recommendations for preventing
osteoporosis

5.7.1 Background

Osteoporosis is a disease affecting many millions of people
around the world. It is characterized by low bone mass and micro-architectural
deterioration of bone tissue, leading to bone fragility and a consequent
increase in risk of fracture (1, 2).

The incidence of vertebral and hip fractures increases
exponentially with advancing age (while that of wrist fractures levels off after
the age of 60 years) (3). Osteoporosis fractures are a major cause of
morbidity and disability in older people and, in the case of hip fractures, can
lead to premature death. Such fractures impose a considerable economic burden on
health services worldwide (4).

5.7.2 Trends

Worldwide variation in the incidence and prevalence of
osteoporosis is difficult to determine because of problems with definition and
diagnosis. The most useful way of comparing osteoporosis prevalence between
populations is to use fracture rates in older people. However, because
osteoporosis is usually not life-threatening, quantitative data from developing
countries are scarce. Despite this, the current consensus is that approximately
1.66 million hip fractures occur each year worldwide, that the incidence is set
to increase four-fold by 2050 because of the increasing numbers of older people,
and that the age-adjusted incidence rates are many times higher in affluent
developed countries than in sub-Saharan Africa and Asia (5-7).

In countries with a high fracture incidence, rates are greater
among women (by three- to four-fold). Thus, although widely regarded in these
countries as a disease that affects women, 20% of symptomatic spine fractures
and 30% of hip fractures occur in men (8). In countries where fracture
rates are low, men and women are more equally affected (7, 9-11). The
incidence of vertebral and hip fractures in both sexes increases exponentially
with age. Hip-fracture rates are highest in Caucasian women living in temperate
climates, are somewhat lower in women from Mediterranean and Asian countries,
and are lowest in women in Africa (9, 10, 12). Countries in economic
transition, such as Hong Kong Special Administrative Region (SAR) of China, have
seen significant increases in age-adjusted fracture rates in recent decades,
while the rates in industrialized countries appear to have reached a plateau
(13, 14).

5.7.3 Diet, physical activity and
osteoporosis

Diet appears to have only a moderate relationship to
osteoporosis, but calcium and vitamin D are both important, at least in older
populations.

Calcium is one of the main bone-forming minerals and an
appropriate supply to bone is essential at all stages of life. In estimating
calcium requirements, most committees have used either a factorial approach,
where calculations of skeletal accretion and turnover rates are combined with
typical values for calcium absorption and excretion, or a variety of methods
based on experimentally-derived balance data (15, 16). There has been
considerable debate about whether current recommended intakes are adequate to
maximize peak bone mass and to minimize bone loss and fracture risk in later
life, and the controversies continue (2, 12, 15-17).

Vitamin D is obtained either from the diet or by synthesis in
the skin under the action of sunlight. Overt vitamin D deficiency causes rickets
in children and osteomalacia in adults, conditions where the ratio of mineral to
osteoid inbone is reduced. Poor vitamin D status in the elderly, at plasma
levels of 25-hydroxyvitamin D above those associated with osteomalacia, has been
linked to age-related bone loss and osteoporotic fracture, where the ratio of
mineral to osteoid remains normal.

Many other nutrients and dietary factors may be important for
long-term bone health and the prevention of osteoporosis. Among the essential
nutrients, plausible hypotheses for involvement with skeletal health, based on
biochemical and metabolic evidence, can be made for zinc, copper, manganese,
boron, vitamin A, vitamin C, vitamin K, the B vitamins, potassium and sodium
(15). Evidence from physiological and clinical studies is largely
lacking, and the data are often difficult to interpret because of potential
size-confounding or bone remodelling transient effects.

5.7.4 Strength of
evidence

For older people, there is convincing evidence for a reduction
in risk for osteoporosis with sufficient intake of vitamin D and calcium
together, and for an increase in risk with high consumption of alcohol and low
body weight. Evidence suggesting a probable relationship, again in older people,
supports a role for calcium and vitamin D separately, but none with
fluoride.

Strength of evidence with fracture as outcome

There is considerable geographical variation in the incidence
of fractures, and cultural variation in the intakes of nutrients associated with
osteoporosis and the clinical outcome of fracture. In Table 18, where the
evidence on risk factors for osteoporosis is summarized, it is important to note
that the level of certainty is given in relation to fracture as the outcome,
rather than apparent bone mineral density as measured by dual-energy X-ray
absorptiometry or other indirect methods. Since the Consultation addressed
health in terms of burden of disease, fractures were considered the more
relevant end-point.

a In populations with high fracture
incidence only. Applies to men and women older than 50-60 years, with a low
calcium intake and/or poor vitamin D status.

b At levels used to fluoridate water supplies. High
fluoride intake causes fluorosis and may also alter bone matrix.

c Several components of fruits and vegetables are
associated with a decreased risk at levels of intake within the normal range of
consumption (e.g. alkalinity, vitamin K, phytoestrogens, potassium, magnesium,
boron). Vitamin C deficiency (scurvy) results in osteopenic bone
disease.

5.7.5 Disease-specific
recommendations

In countries with a high fracture incidence, a minimum of
400-500 mg of calcium intake is required to prevent osteoporosis. When
consumption of dairy products is limited, other sources of calcium include fish
with edible bones, tortillas processed with lime, green vegetables high in
calcium (e.g. broccoli, kale), legumes and by-products of legumes (e.g. tofu).
The interaction between calcium intake and physical activity, sun exposure, and
intake of other dietary components (e.g. vitamin D, vitamin K, sodium, protein)
and protective phytonutrients (e.g. soy compounds), needs to be considered
before recommending increased calcium intake in countries with low fracture
incidence in order to be in line with recommendations for industrialized
countries (18).

With regard to calcium intakes to prevent osteoporosis, the
Consultation referred to the recommendations of the Joint FAO/WHO Expert
Consultation on Vitamin and Mineral Requirements in Human Nutrition (18)
which highlighted the calcium paradox. The paradox (that hip fracture rates are
higher in developed countries where calcium intake is higher than in developing
countries where calcium intake is lower) clearly calls for an explanation. To
date, the accumulated data indicate that the adverse effect of protein, in
particular animal (but not vegetable) protein, might outweigh the positive
effect of calcium intake on calcium balance.

The report of the Joint FAO/WHO Expert Consultation on Vitamin
and Mineral Requirements in Human Nutrition made it clear that the
recommendations for calcium intakes were based on long-term (90 days) calcium
balance data for adults derived from Australia, Canada, the European Union, the
United Kingdom and the United States, and were not necessarily applicable to all
countries worldwide. The report also acknowledged that strong evidence was
emerging that the requirements for calcium might vary from culture to culture
for dietary, genetic, lifestyle and geographical reasons. Therefore, two sets of
allowances were recommended: one for countries with low consumption of animal
protein, and another based on data from North America and Western Europes
(18).

The following conclusions were reached:

There is no case
for global, population-based approaches. A case can be made for targeted
approaches with respect to calcium and vitamin D in high-risk subgroups of
populations, i.e. those with a high fracture incidence.

In countries with high
osteoporotic fracture incidence, a low calcium intake (i.e. below 400-500 mg per
day) (15) among older men and women is associated with increased fracture
risk.

In countries with high
fracture incidence, increases in dietary vitamin D and calcium in the older
populations can decrease fracture risk. Therefore, an adequate vitamin D status
should be ensured. If vitamin D is obtained predominantly from dietary sources,
for example, when sunshine exposure is limited, an intake of 5-10 mg per day is
recommended.

Although firm evidence is
lacking, prudent dietary and some lifestyle recommendations developed in respect
of other chronic diseases may prove helpful in terms of reducing fracture risk.
These include:

- increase physical activity;

- reduce sodium intake;

- increase consumption of fruits and vegetables;

- maintain a healthy body weight;

- avoid smoking;

- limit alcohol intake.

Convincing evidence indicates
that physical activity, particularly activity that maintains or increases muscle
strength, coordination and balance as important determinants of propensity for
falling, is beneficial in prevention of osteoporotic fractures. In addition,
regular lifetime weight-bearing activities, especially in modes that include
impacts on bones and are done in vigorous fashion, increase peak bone mass in
youth and help to maintain bone mass in later life.

References

1. Consensus Development Conference. Diagnosis,
prophylaxis, and treatment of osteoporosis. American Journal of Medicine,
1993, 94:646-650.

2. Prentice A. Is nutrition important in osteoporosis?
Proceedings of the Nutrition Society, 1997, 56:357-367.

4. Johnell O. The socioeconomic burden of fractures:
today and in the 21st century. American Journal of Medicine, 1997,
103(Suppl. 2A):S20-S25.

5. Royal College of Physicians. Fractured neck of
femur. Prevention and management. Summary and recommendations of a report of the
Royal College of Physicians. Journal of the Royal College of Physicians,
1989, 23:8-12.

14. Lau EM, Cooper C. The epidemiology of osteoporosis:
the oriental perspective in a world context. Clinical Orthopaedics and
Related Research, 1996, 323:65-74.

15. Department of Health. Nutrition and bone health:
with particular reference to calcium and vitamin D. Report of the Subgroup on
Bone Health, Working Group on the Nutritional Status of the Population of the
Committee on Medical Aspects of Food and Nutrition Policy. London, The
Stationery Office, 1998 (Report on Health and Social Subjects, No.
49).

[4] A WHO Expert Consultation
on Appropriate BMI for Asian Populations and its Implications for Policy and
Intervention Strategies was held in Singapore from 8 to 11 July 2002 in order
to: (i) review the scientific evidence on the relationship between BMI, body
composition and risk factors in Asian populations; (ii) examine if population
specific BMI cut-off points for overweight and obesity are necessary for Asian
populations; (iii) examine the purpose and basis of ethnic-specific definitions;
and iv) examine further research needs in this area. As one of its
recommendations, the Consultation formed a Working Group to examine available
data on the relationship between waist circumference and morbidity, and the
interaction between BMI, waist circumference and health risk in order to define
future research needs and develop recommendations for the use of additional
waist measurements to further define risks.[5] See also reference
5.[6] The glycaemic index is
calculated as the glycaemic response to a quantity of food containing a set
amount, usually 50 g, of carbohydrate, expressed as a percentage of the
glycaemic response following ingestion of a similar quantity of glucose or of
carbohydrate in white bread.[7] Specific amounts will
depend on the analytical methodologies used to measure fibre.[8] One unit is equivalent to
approximately 10 g of alcohol and is provided by one glass of beer, wine or
spirits.[9] Poultry and fish (except
Chinese-style salted fish) have been studied and found not to be associated with
increased risk for cancer.